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Renal / Genitourinary

Glomerulonephritis

GN Verified · Oct 2026

Glomerulonephritis is inflammatory injury to the glomerular filtration barrier that produces nephritic syndrome — hematuria with red-cell casts, hypertension, oliguria, edema and sub-nephrotic proteinuria — with causes ranging from self-limiting post-infectious disease to rapidly progressive forms that destroy renal function in days.

The disorder behind cola-coloured urine, red-cell casts, the low-C3 clue, the six-weeks-after-impetigo correction, and the hemoptysis that turns a kidney problem into a respiratory emergency.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 The filtration barrier, and what breaks it

Put simply, glomerulonephritis is damage to the glomeruli — the part of the kidney that filters waste and fluid out of the blood. That filter is a three-layer structure: endothelium, glomerular basement membrane (GBM), and podocytes. It is broken in four ways — direct endothelial injury, "deposition of immune complex in the subendothelial, subepithelial, and mesangial spaces," basement-membrane disruption, and podocyte damage — and whichever route is taken, the downstream consequences are the same.

Nephritic syndrome is that consequence set: hematuria, hypertension, oliguria, and edema. The chain is worth following link by link, because every finding on the page hangs off it. Disruption of the barrier "allows red blood cells, albumin, and large molecules to get filtered in the urine," producing hematuria and proteinuria. Inflammation simultaneously reduces the glomerular filtration rate, so salt and water are retained → hypertension and edema, and waste is not cleared → oliguria and azotemia. The filter is leaking and clogging at the same time.

The number that separates nephritic from nephrotic is 3.5 g/day. Nephritic syndrome has proteinuria "in the sub-nephrotic range (less than 3.5 g/day)," though it can exceed this; nephrotic syndrome involves proteinuria exceeding 3.5 g/day. The shorthand: nephritic is blood in the urine with only modest protein; nephrotic is massive protein. And one more framing matters for how the workup is organized — nephritic syndrome "is a common presentation of most proliferative glomerulonephritides." It is a syndrome, not a diagnosis, and the entire job of the investigation is to find which glomerulonephritis is producing it.

The nephritic chain. A leaking, inflamed barrier lets cells and protein out while the falling filtration rate holds salt, water and waste in — and the 3.5 g/day proteinuria line is what separates this from nephrotic syndrome.

02 Three diseases, three timings — and the latency everyone gets wrong

Post-streptococcal glomerulonephritis (PSGN) is "rapid deterioration of kidney function due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection." Nephritogenic strains of group A beta-hemolytic streptococci carry the implicated antigens — the nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B. Immune complexes form "peripherally in the blood or in situ in kidney tissues when antibodies bind to antigens deposited in the glomerular basement membrane," and this "activates the alternative complement pathway, leading to the infiltration of leukocytes." That single mechanistic detail explains the most useful laboratory clue in this disorder: because the alternative pathway is consumed, C3 falls while C4 stays normal. PSGN is "the most common cause of glomerulonephritis in children worldwide."

The latency is the part that is commonly taught wrong. After pharyngitis, sources place the interval at 1–2 weeks or 2–3 weeks — so teach it as about 1 to 3 weeks after a sore throat. But after a skin infection, the interval is far longer: PSGN develops "6 weeks after a skin infection (impetigo)." Applying a one-to-three-week rule to a child who had impetigo a month and a half ago means dismissing the very history that explains the urine. The serology follows the same split — "elevated anti-streptolysin O titers are commonly observed after pharyngitis," which makes ASO the throat marker and anti-DNase B the one that matters after impetigo.

IgA nephropathy (Berger disease) behaves in the opposite way, and the timing is the discriminator. Hematuria arrives with the infection rather than weeks after it: "the co-occurrence of a URI and macroscopic hematuria is so prevalent that it has earned its own designation — synpharyngitic hematuria." Its mechanism is a four-hit sequence: genetically susceptible patients produce abnormally glycosylated IgA1 missing a galactose molecule at the hinge region; that abnormal IgA1 triggers autoantibodies and anti-glycan IgGs; the resulting complexes circulate and deposit in the mesangium; and mesangial cells plus the lectin and alternative complement systems activate, releasing cytokines and driving inflammation and fibrosis. It is "one of the leading causes of glomerulonephritis and renal failure," peaking in the second and third decades of life.

Timing is the bedside discriminator. Hematuria during the infection points to IgA nephropathy; hematuria weeks later points to post-streptococcal disease — and the skin route takes about six weeks, not one to three.

03 Rapidly progressive glomerulonephritis — the crescent clock

Rapidly progressive glomerulonephritis (RPGN) is "rapid loss of renal function over a very short period (days to weeks)" with a nephritic urinalysis and crescent formation on biopsy. It splits into three immunologic types whose shares are worth knowing because they determine the serology ordered: anti-GBM disease 10–15%, immune complex 25–30%, and pauci-immune (ANCA-associated) 40–50% of adult cases — the largest group.

The crescent is the reason this is an emergency rather than a diagnosis. It forms by "GBM rupture followed by extra-capillary fibrin precipitation, the proliferation of parietal cells" — and then the clock runs out: once fibrosis develops, "loss of renal function becomes irreversible." The prognosis data make the timing concrete. Focal disease with more than 50% normal glomeruli shows over 90% renal recovery at 5-year follow-up; disease with more than 50% globally sclerosed glomeruli shows less than 25% renal recovery. Untreated pauci-immune RPGN carries 80% mortality, while aggressive immunosuppression raises survival to 75% at 5 years.

Anti-GBM disease (Goodpasture syndrome) explains why a kidney disease presents with a cough. IgG antibodies target "the non-collagenous domain of the α-3 chain of type IV collagen," an antigen present in both the glomerular and the alveolar basement membrane — so the same antibody attacks lung and kidney simultaneously. Pulmonary involvement occurs in 40–60% of cases, and "hemoptysis and shortness of breath may be the first clinical feature." An inciting lung injury such as smoking appears necessary for the pulmonary manifestations even when antibody is present, which is why smoking, metal dust, organic solvents and hydrocarbons are listed risk factors. Two testing caveats belong with it: approximately 10% of patients with biopsy-confirmed anti-GBM disease have no detectable circulating antibody, so a negative test does not exclude the disease — and 10% to 50% of anti-GBM patients also have detectable ANCA, usually anti-MPO, with dual positivity itself an indication to add plasma exchange (KDIGO 2024 Practice Point 9.3.1.10).

Three immunologic routes converge on one lesion. The crescent is reversible until it fibroses, which is why RPGN is a treat-now diagnosis — and the shared collagen antigen is why anti-GBM disease bleeds into the lungs.

04 Casts, complement and the logic of the workup

The urinalysis is the diagnostic centre of gravity, and one finding on it is close to decisive. "In nephritic syndrome, the urine has greater than 5 RBCs/HPF along with acanthocytes, dysmorphic RBCs, and red blood cell (RBC) casts," against an upper limit of normal of 3 RBCs/HPF. And the key sentence: "dysmorphic RBCs — a feature of glomerular hematuria, acanthocytes, and RBC casts are pathognomonic of glomerulonephritis."

The cast is worth understanding rather than memorizing. "RBC casts are formed when deformed, and distorted RBCs and white blood cells are encased by the Tamm-Horsfall protein," which renal tubular cells secrete normally. The cast is a mould of the tubule — so the blood must have entered the stream above the tubule, at the glomerulus. That is why a red-cell cast rules out the bladder, the prostate and a stone in one step: those bleed downstream of where casts are made.

Complement is the fastest way to narrow the differential. Levels fall "in diseases in which there is an activation of the inflammatory cascade resulting in deposition of immune complexes in the glomerulus," namely post-streptococcal glomerulonephritis, infective endocarditis, and SLE. In PSGN specifically, "C3 levels are typically low during the acute phase and return to normal within 6 to 8 weeks," while C1q and C4 are typically not consumed — the alternative pathway signature. From there the serology panel sorts the rest: ANA and anti-dsDNA for lupus, ANCA for systemic vasculitis (C-ANCA is 90% PR-3 reactive, P-ANCA 90% MPO reactive), anti-GBM for Goodpasture, hepatitis serology, and serum protein electrophoresis for plasma cell disorders. Renal biopsy gives the definitive answer, and the immunofluorescence pattern is itself the diagnosis: mesangial granular IgA means IgA nephropathy; bright linear IgG along the GBM means anti-GBM disease. PSGN is the one cause that generally does not need a biopsy — "unless atypical features are present, such as rapidly progressive glomerulonephritis, normal complement levels, or no rise in antistreptococcal antibodies." Those three exceptions are precisely the red flags that the diagnosis is something worse.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Post-streptococcal glomerulonephritis — the most common cause in children worldwide; nephritogenic group A beta-hemolytic streptococci after pharyngitis (about 1–3 weeks) or impetigo (about 6 weeks) Other infection-related glomerulonephritis — bacterial (meningococcemia, staphylococcal endocarditis, pneumococcal pneumonia), viral (hepatitis B and C, mumps, HIV, varicella, EBV), parasitic (malaria, toxoplasmosis) IgA nephropathy — about 10% of US renal biopsies, up to 40% in East Asia; male predominance 2.5:1 in the US and Europe; peak incidence in the second and third decades Rapidly progressive disease — pauci-immune (ANCA-associated) 40–50% of adult cases, immune complex 25–30%, anti-GBM 10–15% Systemic lupus erythematosus and other immune-complex deposition diseases ANCA vasculitides with their renal involvement rates — granulomatosis with polyangiitis 80%, microscopic polyangiitis 90%, eosinophilic granulomatosis 45% Smoking — a Goodpasture trigger (an inciting lung injury appears necessary for pulmonary disease) and an independent risk for IgA nephropathy progression that worsens as GFR falls modifiable Anti-GBM triggers: exposure to metal dust, organic solvents or hydrocarbons; cocaine inhalation; higher inspired oxygen; extracorporeal shock wave lithotripsy modifiable Infections as anti-GBM triggers — influenza A, bacteremia, endotoxemia; and alemtuzumab Sustained proteinuria of 1 g/day or more in IgA nephropathy — a 46-fold increased risk of end-stage renal disease versus under 500 mg/day modifiable Sustained hypertension, and Oxford MEST-C findings — mesangial hypercellularity, endocapillary hypercellularity, segmental sclerosis, tubular atrophy/interstitial fibrosis and crescents — of which tubular atrophy or interstitial fibrosis is most predictive of poor prognosis modifiable Obesity and East Asian origin (IgA nephropathy progression); certain malignancies, including myeloproliferative disease Bimodal age risk in anti-GBM disease — around the third and sixth decades, with younger patients getting simultaneous pulmonary-renal disease and those over 50 more often renal-limited

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Cola-coloured, tea-coloured or smoky urine — the signature finding early Hold & notify
Why: Red cells crossing a broken filtration barrier; the brown colour is concentrated blood rather than fresh bleeding. Gross hematuria occurs in 30% to 50% of post-streptococcal cases. Patient wording: "dark, rust-colored, or brown urine." Always a hold-notify finding when new.
Hypertension — up to 80% of post-streptococcal patients Hold & notify
Why: Salt and water retained behind a fallen glomerular filtration rate. In PSGN it "resolves in most cases within 10 days," which is a useful expectation to set — but severe hypertension is a different matter entirely and can progress to hypertensive emergency.
Periorbital and pedal edema — in 65% to 90% of post-streptococcal cases Hold & notify
Why: The same salt and water retention. Facial and periorbital puffiness that is worst in the morning is the classic paediatric presentation. Note the severity marker: "generalized edema often indicat[es] more severe disease."
Oliguria and azotemia Hold & notify
Why: Directly reflects the fallen filtration rate. Falling urine output is the single most sensitive bedside trend on this page — it is the earliest quantitative sign that the kidney is losing ground, and anuria is an explicit poor-prognosis marker in rapidly progressive disease.
Foamy urine Expected
Why: Sub-nephrotic proteinuria — under 3.5 g/day — "may cause foamy urine when protein content is high." Its presence with hematuria fits nephritic syndrome; proteinuria beyond 3.5 g/day would move the diagnosis toward nephrotic syndrome instead.
Jugular venous distension, pitting edema and crackles on chest auscultation Hold & notify
Why: Fluid overload that has reached the lungs. Also seen are pallor and anemia. Crackles change the urgency — the retained volume is no longer confined to the interstitium, and this is the point at which loop diuretics and fluid restriction stop being routine and become time-sensitive.
About 50% of post-streptococcal cases are asymptomatic, found on routine urinalysis Expected
Why: The glomerular injury does not require symptoms to be present or progressive. This is why screening urinalysis after a streptococcal infection finds disease that the history never would — the test, not the symptom, makes the diagnosis in half of cases.
Gross hematuria arriving during an upper respiratory infection — synpharyngitic hematuria Expected
Why: The IgA nephropathy signature. It occurs concurrently with or shortly after the infection rather than weeks later, which is the bedside discriminator from post-streptococcal disease. Up to 35% of IgA nephropathy patients also have GI symptoms — abdominal pain, cramping, diarrhea — and fewer than 5% present with acute kidney injury.
Hemoptysis or new shortness of breath with an active urinary sediment Report immediately
Why: Pulmonary-renal syndrome until proven otherwise. The alveolar and glomerular basement membranes share the α-3 chain of type IV collagen, so one antibody attacks both. Hemoptysis ranges from subtle to life-threatening, with dyspnea, tachypnea, basilar inspiratory crackles and cyanosis — and it "may be the first clinical feature."
Fevers, night sweats, weight loss, arthralgias, oral ulceration, scleritis, epistaxis, sinusitis, palpable purpura Report immediately
Why: The vasculitis clue set. These findings mean systemic disease rather than a self-limiting nephritis, and they belong to the ANCA-associated vasculitides that make up the largest share of adult rapidly progressive glomerulonephritis.
Seizures or altered consciousness with high blood pressure Report immediately
Why: Hypertensive encephalopathy — a listed complication of nephritic syndrome and a named acute-phase complication of post-streptococcal disease. The blood pressure that seemed like a number to monitor has become the thing causing neurologic injury.
Generalized muscle weakness or flaccid paralysis Report immediately
Why: Hyperkalemia, a listed complication of nephritic syndrome, from potassium the failing kidney cannot excrete. Symptoms typically appear above 6.0 mEq/L — well past the point where the ECG has already begun to change.
Rapid loss of renal function over days to weeks late Report immediately
Why: Rapidly progressive glomerulonephritis. Crescents are forming, and once fibrosis develops, "loss of renal function becomes irreversible." Higher creatinine at presentation, anuria or dialysis dependence all predict a poor outcome — which makes the speed of recognition part of the treatment.

Diagnostics

Test In this disorder Normal
Urinalysis with microscopy "Dysmorphic RBCs… acanthocytes, and RBC casts are pathognomonic of glomerulonephritis." The cast is a mould of the tubule, formed when distorted red cells are encased in Tamm-Horsfall protein — so the bleeding must have started above the tubule, at the glomerulus, which rules out a bladder, prostatic or stone source in a single step More than 5 RBCs/HPF with acanthocytes, dysmorphic RBCs and red blood cell casts, occasionally white cell casts Upper limit of normal is 3 RBCs/HPF
Complement C3 and C4 The low C3 with normal C4 pattern is the alternative-pathway signature and the fastest way to narrow the differential. Its corollary is a red flag: normal complement in a suspected PSGN is one of the three reasons to biopsy, because it means the diagnosis is something else Low in immune-complex disease — post-streptococcal glomerulonephritis, infective endocarditis and SLE. In PSGN, C3 is low in the acute phase and returns to normal within 6 to 8 weeks, with C1q and C4 typically not consumed —
Streptococcal serology — ASO and anti-DNase B Match the marker to the route. "Elevated anti-streptolysin O titers are commonly observed after pharyngitis" — so ASO is the throat marker, and anti-DNase B is the one that matters after impetigo. No rise in antistreptococcal antibodies is the second of the three reasons to biopsy a suspected PSGN High titres "indicate a recent streptococcal infection"; anti-hyaluronidase is also used —
Autoimmune serology panel Two caveats prevent false reassurance. About 10% of patients with biopsy-confirmed anti-GBM disease have no detectable circulating antibody, so a negative test does not exclude it. And 10% to 50% of anti-GBM patients also carry ANCA, usually anti-MPO — dual positivity is itself an indication to add plasma exchange (KDIGO 2024 Practice Point 9.3.1.10) ANA and anti-dsDNA (highly sensitive for SLE); ANCA — C-ANCA is 90% PR-3 reactive, P-ANCA 90% MPO reactive; anti-GBM antibodies; hepatitis B and C serology; serum protein electrophoresis —
Renal function and proteinuria quantification The proteinuria number carries prognostic weight in IgA nephropathy: sustained proteinuria of 1 g/day or more confers a 46-fold increased risk of end-stage renal disease compared with under 500 mg/day. It is also the only validated early biomarker for guiding treatment decisions — so it appears as two different numbers that must not be confused. Treatment target: keep proteinuria below 0.5 g/day, ideally below 0.3 g/day (KDIGO 2025 IgA nephropathy guideline), accepting that extensive scarring may make that unreachable. Threshold to consider IgA-targeted treatment (Nefecon, or a reduced-dose glucocorticoid where Nefecon is unavailable): proteinuria of 0.5 g/day or more, on or off treatment (KDIGO 2025). The overall aim is to slow loss of kidney function to the physiological rate, under about 1 mL/min per year in most adults Plasma creatinine and urea, with creatinine used to estimate GFR and stage the disease; proteinuria quantified by protein-to-creatinine ratio or 24-hour urinary protein KDIGO 2025 IgA nephropathy guideline —
Renal biopsy with immunofluorescence Biopsy "will provide the definite underlying cause," and in RPGN "histological diagnosis through renal biopsy is the mainstay." PSGN is the exception — generally no biopsy is needed "unless atypical features are present, such as rapidly progressive glomerulonephritis, normal complement levels, or no rise in antistreptococcal antibodies." Note also that serum IgA level is not a diagnostic test — it lacks "sensitivity and specificity for IgAN diagnosis". In IgA nephropathy the biopsy is scored by the revised Oxford MEST-C classification — mesangial hypercellularity, endocapillary hypercellularity, segmental sclerosis, tubular atrophy/interstitial fibrosis, and crescents. Crescents are a formal component of that score, but KDIGO finds "insufficient evidence to base treatment decisions solely on the presence and number of cellular/fibrocellular crescents," and crescents without a concomitant change in serum creatinine "do not constitute rapidly progressive IgAN" — the rate of change in eGFR is what the histology must be read against The pattern is the diagnosis: mesangial granular IgA = IgA nephropathy; bright linear IgG and C3 along the GBM = anti-GBM disease; crescents = rapidly progressive glomerulonephritis —
Serum potassium with ECG ECG progression: peaked T waves at 5.5–6.5 mEq/L, flattening or loss of P waves at 6.5–7.5, QRS widening at 7–8, and severe arrhythmias with a sine-wave pattern at 8–10. The heralding cue in this disorder is simple — falling urine output with a rising potassium Hyperkalemia is a listed complication; the threshold is above 5.0–5.5 mEq/L, and symptoms appear above 6.0 mEq/L —
Chest imaging in suspected pulmonary-renal syndrome "The apices and costophrenic angles are generally spared" — a distribution detail that helps separate alveolar hemorrhage from pneumonia or pulmonary edema in a patient who is already in renal failure "Patchy parenchymal opacifications, which are usually bilateral and bibasilar" —

Complications

Warning: Pulmonary-renal syndrome and alveolar hemorrhage Report immediately
Hemoptysis with an active urinary sediment, ranging from subtle to life-threatening, with dyspnea, tachypnea, basilar crackles and cyanosis. Pulmonary involvement occurs in 40% to 60% of anti-GBM disease, and "may be the first clinical feature."
The alveolar and glomerular basement membranes share the α-3 chain of type IV collagen, so a single autoantibody attacks both organs. Pulmonary hemorrhage may require mechanical ventilation. Plasma exchange is indicated — but the two diseases are governed by opposite logics. In ANCA-associated vasculitis, severity decides: the KDIGO 2024 ANCA guideline (Practice Point 9.3.1.9) says consider plasma exchange for (1) serum creatinine above 3.4 mg/dL (> 300 μmol/L), (2) a dialysis requirement or a rapidly rising creatinine, or (3) diffuse alveolar hemorrhage with hypoxemia. In anti-GBM disease, futility decides — which is why no creatinine threshold exists on that side. KDIGO 2021 Recommendation 11.2.1 recommends cyclophosphamide, glucocorticoids and plasmapheresis for all patients with anti-GBM glomerulonephritis except those meeting all three of: treated with dialysis at presentation, 100% crescents or more than 50% global glomerulosclerosis on an adequate biopsy, and no pulmonary hemorrhage. Read that carefully — dialysis at presentation is one leg of an exclusion, not an indication, and pulmonary hemorrhage overrides the exclusion entirely, so a dialysis-dependent patient with 100% crescents is still treated if they are bleeding into their lungs. The two arms meet in one rule: KDIGO 2024 Practice Point 9.3.1.10 adds plasma exchange for an overlap syndrome of ANCA-associated vasculitis and anti-GBM disease, which is why the dual-antibody result in the serology panel changes management rather than merely labelling it. Any hemoptysis in a patient with glomerulonephritis is treated as this until proven otherwise.
Warning: Hypertensive emergency and encephalopathy Report immediately
"Hypertensive encephalopathy presenting as seizures and altered consciousness" is a listed complication of nephritic syndrome, and hypertensive emergency is a named acute-phase complication of post-streptococcal disease alongside fluid overload and acute kidney failure needing replacement therapy.
Up to 80% of post-streptococcal patients are hypertensive, and while it "resolves in most cases within 10 days," the interval between presentation and resolution is exactly when the encephalopathy happens. The management sequence matters: salt restriction, fluid restriction and a loop diuretic come first, with an antihypertensive added for blood pressure that stays elevated despite them.
Warning: Hyperkalemia and the electrolyte set Report immediately
Nephritic syndrome complications include hyperkalemia, hyperphosphatemia, hypocalcemia, azotemia and heart failure. Hyperkalemia begins above 5.0–5.5 mEq/L, and symptoms — generalized muscle weakness, flaccid paralysis — appear above 6.0 mEq/L.
The ECG is the action trigger rather than the number alone: peaked T waves at 5.5–6.5 mEq/L, loss of P waves at 6.5–7.5, QRS widening at 7–8, and a sine-wave pattern at 8–10. In a patient whose urine output is falling, the potassium is the value that turns a slow renal problem into an immediate cardiac one, which is why dietary potassium restriction sits beside sodium restriction on this page.
Warning: Progression to rapidly progressive glomerulonephritis Report immediately
Acute renal failure with rapid loss of renal function over days to weeks. Once fibrosis develops, "loss of renal function becomes irreversible."
The outcome is a direct function of how early treatment starts. Focal disease with more than 50% normal glomeruli shows over 90% renal recovery at 5 years; disease with more than 50% globally sclerosed glomeruli shows under 25%. Untreated pauci-immune disease carries 80% mortality, and aggressive immunosuppression raises survival to 75% at 5 years. In anti-GBM disease the presenting creatinine is decisive: below 5.7 mg/dL, 1- and 5-year survival were 95% and 94%, while dialysis-dependent patients at presentation had only 8% recovery of renal function at 1 year. That figure is the reason treatment decisions in anti-GBM disease turn on futility rather than severity — it is the logic the exclusion rule encodes, and why pulmonary hemorrhage still overrides it.
Caution: Chronic kidney disease — and why age decides
"Children have an acute self-limiting course of glomerulonephritis, and the prognosis is good. Adults typically have a chronic fulminating course. The disease is not resolved in 20% to 74% of adults."
In post-streptococcal disease specifically, complete recovery is observed in the majority of children, while residual hypertension and chronic kidney disease occur in 30% to 50% of affected adults. In IgA nephropathy, 20% to 50% develop end-stage renal disease within 20 years, though up to 50% experience a benign course, with 10-year renal survival between 57% and 91%. A further consideration for treatment complications: patients on high-dose steroids, cyclophosphamide or rituximab face opportunistic infections that "can sometimes be life-threatening."

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

ACE Inhibitors First-line
Cardiovascular · lisinopril

First-line for the proteinuric, hypertensive glomerulonephritis — they lower blood pressure and reduce proteinuria at the same time, which matters because proteinuria is itself the strongest modifiable predictor of progression. Stated directly: "first-line agents for managing proteinuria and lowering blood pressure in IgAN patients typically involve angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)," and in severe nephritic hypertension "ACE inhibitors, ARBs, and nifedipine" are used. Two guideline numbers steer the titration. The KDIGO 2025 IgA nephropathy guideline sets a blood-pressure target of ≤ 120/70 mm Hg — note it is now combined systolic and diastolic, not a systolic figure alone — "using a RASi as the first-choice drug," paired with sodium restriction under 2 g/day; textbook-level targets of 130/80, or under 125 systolic when proteinuria exceeds 1 g/day, sit alongside it as the older framing. The second number is the treatment target for proteinuria itself: maintain it below 0.5 g/day, and ideally below 0.3 g/day, accepting that extensive kidney scarring may make that unreachable — proteinuria being "the only validated early biomarker to help guide clinical decision-making." Do not confuse that target with the threshold for starting a glucocorticoid, which under KDIGO 2025 is proteinuria of 0.5 g/day or more despite supportive care — the point at which IgA-targeted therapy is added alongside, not instead of, the ACE inhibitor or ARB. The payoff for taking supportive care seriously is quantified — in the STOP-IgAN trial, about one-third of patients achieved satisfactory outcomes without any immunosuppression after a 6-month trial of optimized conservative measures including aggressive ACE inhibitor or ARB titration.
Diuretics First-line
Cardiovascular

The loop diuretic is the first pharmacologic step for the volume overload that drives the hypertension, not an afterthought to it. "Loop diuretics may be administered to excrete excess sodium and water retained in the body," and the sequencing rule is explicit: antihypertensives are added only for blood pressure that stays elevated "despite dietary salt, fluid restriction, and loop diuretics." That ordering is the whole logic of nephritic hypertension — the pressure is a volume problem first, so removing the volume is the first-line treatment. The same applies in post-streptococcal disease, where "restriction of dietary sodium intake and loop diuretics may be used to manage hypervolemia and hypertension," with calcium channel blockers added for additional control. Watch the electrolytes as the diuresis proceeds, since hyperkalemia, hyperphosphatemia and hypocalcemia are already listed complications of the underlying disease.
Corticosteroids
Endocrine · prednisone

The role is inflammation control, and it is disease-specific rather than universal — which is where most errors are made. Generally, corticosteroids "help relieve the inflammation in the kidney and promote healing," and immunosuppression "is most useful for rapidly progressive glomerulonephritis." In RPGN they are urgent and empirical: intravenous methylprednisolone 500 mg or 1 g for a minimum of 3 doses, and in anti-GBM disease 1 g daily for 3 days followed by oral prednisolone 1 mg/kg/day (maximum 60 mg), reduced weekly to 20 mg by 6 weeks and tapered off by 6 months. In IgA nephropathy they are conditional and now second-choice: the KDIGO 2025 IgA nephropathy guideline suggests a 9-month course of targeted-release budesonide (Nefecon) for patients at risk of progression (proteinuria ≥ 0.5 g/day), and where that is unavailable, a reduced-dose systemic glucocorticoid for 6–9 months with antimicrobial prophylaxis. And in post-streptococcal glomerulonephritis they are not indicated at all: "there is no definite recommendation for the use of immunosuppressive therapies," and KDIGO’s position is that "the role of glucocorticoids and other immunosuppression is unproven." PSGN is treated supportively. Where steroids are used, monitor for opportunistic infection, which is a named and sometimes life-threatening complication.

Beyond medications

  • Sodium restriction, fluid restriction and reduced activity are the first interventions. "To relieve the existing edema and minimize the risk of developing edema, fluid restriction is advised," and "patients should have a diet low in sodium and potassium" — the potassium because hyperkalemia is a listed complication, the sodium because it drives the water retention. The KDIGO 2025 IgA nephropathy guideline puts a figure on it: under 2 g/day — unchanged from the KDIGO 2021 edition, which also gave it as under 90 mmol/day. Patients are also "advised to have reduced physical activity along with the treatment" during the acute phase.
  • Antibiotics in post-streptococcal disease do a different job than most people assume. Penicillin (erythromycin if penicillin-allergic) is given to eradicate a still-active or residual streptococcal infection and to limit spread to contacts — but "antibiotics are not indicated [for the nephritis itself], as the infection usually resolves by the time kidney injury develops." By the time the urine turns cola-coloured, the injury is immune-complex-mediated and antibiotics will not reverse it. Say that plainly to families who expect the antibiotic to fix the kidney.
  • Plasma exchange — severity gates one disease, futility gates the other. In ANCA-associated vasculitis, severity decides. The KDIGO 2024 ANCA guideline, Practice Point 9.3.1.9, gives three separate criteria: consider plasma exchange for (1) serum creatinine above 3.4 mg/dL (> 300 μmol/L), (2) a dialysis requirement or a rapidly increasing creatinine, or (3) diffuse alveolar hemorrhage with hypoxemia. The threshold sits where it does because a PEXIVAS post-hoc analysis found an absolute 12-month kidney-failure risk reduction of 4.6% at a creatinine of 3.4–5.7 mg/dL and 6% above 5.7 — the benefit begins well below the older cut-off. In anti-GBM disease, futility decides, and there is deliberately no creatinine threshold at all. KDIGO 2021 Recommendation 11.2.1 recommends cyclophosphamide, glucocorticoids and plasmapheresis for all patients with anti-GBM glomerulonephritis except those who meet all three of: treated with dialysis at presentation; 100% crescents or more than 50% global glomerulosclerosis on an adequate biopsy; and no pulmonary hemorrhage. Two traps in that sentence: dialysis at presentation is a leg of the exclusion, never an indication, and pulmonary hemorrhage overrides the exclusion, so the dialysis-dependent patient with 100% crescents who is bleeding into the lungs is still treated. Start on suspicion — "treatment for anti-GBM disease should start without delay if this diagnosis is suspected, even before the diagnosis is confirmed" (KDIGO 2021 Practice Point 11.2.1). Spanning both diseases: KDIGO 2024 Practice Point 9.3.1.10 adds plasma exchange for an ANCA / anti-GBM overlap syndrome. Mechanics: 4 L per exchange over 2 to 4 weeks, usually with 5% albumin replacement, though fresh frozen plasma (0.3–2 L) is used for invasive procedures or when pulmonary hemorrhage is present — and the endpoint is a titre, not a calendar: "plasma exchange should be performed until anti-GBM titers are no longer detectable" (KDIGO 2021 Practice Point 11.2.2). Note the built-in hazard: removing clotting factors increases bleeding risk.
  • Dialysis and kidney replacement therapy for the fulminant course — in post-streptococcal disease, "in cases with severe kidney dysfunction to manage electrolyte and acid-base imbalances." Dialysis access should be arranged proactively in rapidly progressive disease, with transplant referral coordinated for end-stage disease.
  • IgA nephropathy lifestyle measures carry real weight because a third of patients need nothing more: salt restriction, lipid management, weight loss, smoking cessation — "advising patients to quit smoking is essential," because smoking independently increases the risk of progression — a low-antigen diet restricting gluten, meat and dairy, and low-protein diets, which "may slow the deterioration of renal function." Tonsillectomy is not standard care: its efficacy "has not been consistently demonstrated in randomized controlled trials, leading to its exclusion from standard care guidelines in many regions, particularly outside of Asia."
  • Community-level prevention of post-streptococcal disease is a genuine nursing intervention: "avoiding overcrowded environments and maintaining personal hygiene are crucial measures"; "prompt diagnosis and treatment of throat or skin infections is vital in preventing spread and possibly kidney complications"; and "encouraging the screening of all close contacts and family members to rule out an acute infection is key." Most other forms of glomerulonephritis cannot be prevented, though limiting exposure to solvents and NSAIDs may help.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Run the sourced monitoring set every shift: fluid and salt intake, edema, blood pressure, serum creatinine, potassium levels, and urine output.
Why: This single guideline-level list is the care plan for the whole disorder — every item is either a driver of the disease (salt, fluid), a consequence of it (edema, blood pressure), or an early marker of decompensation (creatinine, potassium, urine output).
Record daily weights and strict intake and output, and treat a falling urine output as the earliest quantitative warning.
Why: Oliguria directly reflects the falling filtration rate, and anuria is an explicit poor-prognosis marker in rapidly progressive disease. Weight detects retained fluid before edema is visible, which is what makes the fluid restriction measurable rather than aspirational.
Treat urine colour as a trend, not a one-off symptom — note whether cola, tea or smoky urine is clearing, darkening, or returning after having cleared.
Why: Returning hematuria in a treated patient is a named relapse cue, alongside edema and hypertension. In IgA nephropathy, gross hematuria recurring with each upper respiratory infection is the disease’s characteristic rhythm rather than a new problem.
Check the potassium alongside the urine output, and obtain an ECG when it rises — escalating on any hyperkalemic change.
Why: A kidney that cannot excrete potassium turns a slow renal problem into an immediate cardiac one. Peaked T waves appear at 5.5–6.5 mEq/L, well before the muscle weakness that patients report above 6.0 — so the ECG change is the action trigger.
Auscultate the chest and assess jugular venous pressure on every assessment, not only when the patient reports breathlessness.
Why: Crackles and JVD mean the retained volume has reached the lungs. And separately, any hemoptysis with an active urinary sediment is a pulmonary-renal syndrome until proven otherwise — an emergency that may present before the kidney findings are appreciated.
Ask specifically when the hematuria began relative to the infection, and about a skin infection as well as a sore throat.
Why: Timing is the bedside discriminator. Hematuria with the infection suggests IgA nephropathy; 1 to 3 weeks after pharyngitis or about 6 weeks after impetigo suggests post-streptococcal disease. A history of impetigo a month and a half ago is easy to dismiss and is exactly the history that explains the urine.
Interventions & safety
Implement the sequence in order: dietary salt restriction and fluid restriction first, then the loop diuretic, and an antihypertensive only if the pressure stays elevated despite both.
Why: Nephritic hypertension is a volume problem before it is a vascular one, so removing the volume is first-line treatment. The sequencing is stated explicitly — antihypertensives are for blood pressure elevated "despite dietary salt, fluid restriction, and loop diuretics."
Restrict dietary potassium alongside sodium.
Why: "Patients should have a diet low in sodium and potassium." The sodium limits water retention; the potassium limit exists because hyperkalemia is a listed complication of nephritic syndrome and the failing kidney cannot clear the load.
Give antibiotics in post-streptococcal disease as infection eradication and contact protection — and do not present them as treatment for the kidney injury.
Why: By the time the nephritis appears, the damage is immune-complex-mediated and "the infection usually resolves by the time kidney injury develops." Framing the antibiotic accurately prevents families from concluding that treatment has failed when the urine stays dark.
Escalate immediately for hemoptysis, new dyspnea, seizures or altered consciousness with high blood pressure, anuria, or a rapidly rising creatinine.
Why: Each maps to a specific emergency: pulmonary-renal syndrome, hypertensive encephalopathy, and rapidly progressive glomerulonephritis. In RPGN the crescents fibrose and "loss of renal function becomes irreversible," so recognition speed is part of the treatment rather than a preliminary to it.
Monitor for infection in every patient on high-dose steroids, cyclophosphamide or rituximab, and treat fever in an immunosuppressed patient as an escalation trigger.
Why: Opportunistic infections are a named treatment complication that "can sometimes be life-threatening." Infection prevention on this page has two faces — preventing the streptococcal trigger, and preventing the complication of the immunosuppression used to treat the result.
Support reduced physical activity during the acute phase, and reintroduce activity as the hematuria, hypertension and edema settle.
Why: Patients "are advised to have reduced physical activity along with the treatment." Setting the expectation early — and naming the resolution markers — prevents both premature return to full activity and unnecessary prolonged restriction after recovery.
Patient teaching
Set the prognosis honestly and by age: children usually recover completely; adults often do not, with residual hypertension and chronic kidney disease in 30–50% of adults after post-streptococcal disease.
Why: "Children have an acute self-limiting course… Adults typically have a chronic fulminating course. The disease is not resolved in 20% to 74% of adults." A family told only that this resolves will not attend the follow-up that an adult patient genuinely needs.
Teach the relapse and warning cues explicitly: hematuria, edema, hypertension — and hemoptysis.
Why: Patients are taught to recognize "symptoms of possible relapse such as hematuria, edema, or hypertension," and RPGN education tells them to "seek medical help in case of decreased urine output, blood in the urine, shortness of breath, hemoptysis." These are the findings a patient can detect at home weeks before a scheduled clinic visit.
Teach the diet as three numbers and one habit: sodium under 2 g/day, restricted potassium, a fluid restriction — and, in IgA nephropathy, smoking cessation.
Why: The sodium figure is the KDIGO 2025 IgA nephropathy target and is what makes the blood-pressure goal achievable. Stopping smoking is essential in IgA nephropathy because smoking independently increases progression risk and worsens as GFR declines.
Explain why the blood-pressure medication continues after the patient feels well, naming the proteinuria link.
Why: ACE inhibitors and ARBs reduce proteinuria as well as blood pressure — and sustained proteinuria of 1 g/day or more carries a 46-fold increased risk of end-stage renal disease versus under 500 mg/day. The drug is protecting the kidney, not just the number on the cuff.
For IgA nephropathy, teach that "a minor URI… can trigger the disease in genetically susceptible patients," and cover the nature of the disease, the possible progression to end-stage disease, the adverse effects of steroid therapy, and the importance of regular follow-up.
Why: Recurrent visible hematuria with every cold is frightening and predictable in equal measure; naming it in advance converts an alarming event into an expected one. Naming the steroid side effects in advance is what sustains adherence when they appear.
Teach household-level prevention after post-streptococcal disease: prompt treatment of throat and skin infections, personal hygiene, avoiding overcrowding, and screening close contacts and family members.
Why: These are stated preventive measures, and they matter more than they sound — the disease is the most common cause of glomerulonephritis in children worldwide, and the same nephritogenic strain circulating in a household can produce another case.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues assemble into one recognizable picture. Cola-coloured urine with 3+ blood and red blood cell casts; periorbital puffiness worst in the morning with ankle edema and a 1.8 kg weight gain; hypertension at 142/90 against a 95th percentile of 127/82; a creatinine that has nearly doubled from his own baseline; and the timing — about 2.5 weeks after a sore throat. The laboratory pair that names the disease is low C3 with a normal C4, alongside an elevated ASO titre. Two findings are reassuring rather than alarming: the chest is clear, and there is no hemoptysis, no rash, no joint swelling and no systemic vasculitis cluster.

  2. 2
    Analyze cues

    This is nephritic syndrome from post-streptococcal glomerulonephritis, and every finding maps to the chain. The broken filtration barrier lets red cells and protein through — hence the hematuria and the 1.1 g/day proteinuria, which sits below the 3.5 g/day nephrotic threshold and therefore fits nephritic rather than nephrotic syndrome. The red blood cell casts are close to decisive: a cast is a mould of the tubule formed from Tamm-Horsfall protein, so the bleeding began above the tubule at the glomerulus — not from a bladder, a stone or trauma. The falling filtration rate retains salt and water, producing the hypertension (present in up to 80% of PSGN cases) and the edema (65–90%), and raises the creatinine. The complement pattern is the mechanism showing itself: the immune complexes activate the alternative pathway, so C3 is consumed and C4 is spared. The timing fits the throat route, and the ASO is the correct marker for pharyngitis — had the history been impetigo, the interval would have been about 6 weeks and anti-DNase B would have been the marker to check.

  3. 3
    Prioritize

    Rank by what can harm him fastest. Priority one is the blood pressure, because hypertensive emergency with encephalopathy — seizures and altered consciousness — is the named acute-phase complication of this disease. Priority two is volume: weight, intake and output, and the edema, because generalized edema indicates more severe disease and crackles would mean it has reached the lungs. Priority three is the potassium and creatinine trend, since hyperkalemia is a listed complication and the creatinine is already moving. Priority four is watching for the features that would mean this is not ordinary PSGN. The proteinuria of 1.1 g/day is worth noting but is not the acute threat.

  4. 4
    Generate solutions

    Start with what needs no prescription: dietary sodium restriction, fluid restriction, and a low-potassium diet, with daily weights and strict intake and output. Anticipate a loop diuretic as the first pharmacologic step, and an antihypertensive added only if the pressure stays elevated despite salt restriction, fluid restriction and the diuretic — that ordering is the point, because this hypertension is a volume problem. Anticipate penicillin if there is any residual or active streptococcal infection, and be ready to explain what it is for: it eradicates the organism and protects contacts, but it will not reverse the kidney injury, which is already immune-mediated. Advise reduced physical activity during the acute phase. Do not anticipate steroids — immunosuppression is unproven in PSGN. Do not anticipate a biopsy either, unless one of the three red flags appears: rapidly progressive disease, normal complement, or no rise in antistreptococcal antibodies. Screen the household contacts.

  5. 5
    Take action

    Teach the family first, because most of this treatment happens at home: the salt, potassium and fluid limits; daily weights; and the specific reasons to call — less urine, worsening puffiness, breathlessness, headache, and above all any seizure or confusion. Then the handover: "13-year-old, 2.5 weeks after pharyngitis, with cola-coloured urine, red cell casts, 3+ blood and 2+ protein, periorbital and ankle edema with 1.8 kg weight gain, BP 142/90 above his 95th percentile, creatinine 0.9 from a baseline of 0.5, low C3 with normal C4 and an elevated ASO. This is post-streptococcal glomerulonephritis. Salt, potassium and fluid restriction started, daily weights and strict intake and output in place. Requesting review for a loop diuretic and blood-pressure management, and contact screening." The traps to name: do not request steroids, do not describe the antibiotic as treating the kidney, and do not reassure with a normal complement — a normal C3 here would mean the diagnosis is wrong.

  6. 6
    Evaluate

    Success over the next weeks has a documented shape. The hypertension resolves in most cases within about 10 days; the edema and weight settle as the diuresis proceeds; urine output rises; the creatinine returns toward his 0.5 mg/dL baseline; and the urine lightens, though microscopic hematuria may linger. The single most useful confirmatory event comes later: C3 returns to normal within 6 to 8 weeks. If it does not, or if his function deteriorates rapidly, that is the trigger to biopsy. Reinforce at the follow-up that complete recovery is expected in the majority of children — while noting that the same disease in an adult would carry a 30–50% risk of residual hypertension and chronic kidney disease, which is why the adult pathway looks so different.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Paediatric clinic · 1015, a same-day appointment booked by the school nurse

A 13-year-old boy brought in because his urine has been "the colour of Coke" for two days. His mother reports he had a sore throat about two and a half weeks ago that was treated at an urgent-care clinic. She says his face has looked "puffy, especially first thing in the morning" for the last three or four days, and that he has been tired and off his food.

Vitals — BP 142/90 (95th percentile for age and height is 127/82) · HR 88 · RR 18 · T 36.8 °C · weight up 1.8 kg from a routine visit six weeks ago
Assessment — periorbital puffiness bilaterally · mild pitting edema at both ankles · chest clear on auscultation · no rash, no joint swelling, no hemoptysis
Urinalysis — dark brown urine · blood 3+, protein 2+ · microscopy: more than 5 RBCs per high-power field, dysmorphic RBCs, red blood cell casts
Labs — creatinine 0.9 mg/dL (baseline 0.5) · potassium 4.6 mEq/L · C3 low, C4 normal · ASO titre elevated · urine protein-to-creatinine ratio corresponding to about 1.1 g/day
History — sore throat about 2.5 weeks ago · no skin lesions reported · no family history of kidney disease
Q1 Select all that apply
Which findings support post-streptococcal glomerulonephritis rather than another cause? Select all that apply.
  1. A. Low C3 with a normal C4
  2. B. Hematuria beginning about 2.5 weeks after pharyngitis
  3. C. Red blood cell casts on urine microscopy
  4. D. Proteinuria of about 1.1 g/day
  5. E. Elevated anti-streptolysin O titre
Reveal answer & rationale
Answer: A, B, E
Immune complexes in post-streptococcal disease activate the alternative complement pathway, so C3 is consumed while C4 is spared — a pattern specific enough that a normal complement is one of the three reasons to biopsy (A). A latency of about one to three weeks after pharyngitis fits, and distinguishes this from synpharyngitic IgA nephropathy, where hematuria arrives with the infection (B). An elevated ASO titre indicates recent streptococcal infection and is the correct marker for the throat route (E). Red blood cell casts (C) confirm that the bleeding is glomerular but do not identify which glomerulonephritis — they are pathognomonic of glomerulonephritis in general. Proteinuria of 1.1 g/day (D) is consistent with nephritic syndrome because it is under the 3.5 g/day threshold, but it is equally consistent with several other causes.
Q2 Multiple choice
The mother asks whether her son will need steroids for his kidneys. The best response is:
  1. A. "Yes — corticosteroids are standard treatment to reduce the kidney inflammation."
  2. B. "No — for this type of kidney inflammation the treatment is supportive, because immunosuppression has not been shown to help."
  3. C. "Only if his protein level rises above 3.5 grams a day."
  4. D. "Steroids will be started if the antibiotic does not clear the blood from his urine."
Reveal answer & rationale
Answer: B
For post-streptococcal glomerulonephritis, "there is no definite recommendation for the use of immunosuppressive therapies," and the KDIGO position (via the CARI commentary) is that "the role of glucocorticoids and other immunosuppression is unproven" — management is salt and fluid restriction, a loop diuretic and blood-pressure control (B). Option A states the widely believed opposite. Option C invents a trigger and confuses the nephritic/nephrotic threshold with a treatment indication; the sourced treatment threshold belongs to IgA nephropathy — proteinuria of 0.5 g/day or more despite supportive care (KDIGO 2025). Option D compounds two errors: antibiotics do not clear the hematuria, because the injury is already immune-complex-mediated by the time the urine darkens.
Q3 Put in order
Put the nurse’s first four actions in priority order:
  1. A. Notify the provider with the blood pressure, creatinine trend and complement results
  2. B. Recheck the blood pressure and assess for headache, visual change or altered mental status
  3. C. Start daily weights, strict intake and output, and sodium, potassium and fluid restriction
  4. D. Teach the family the call-back triggers, including reduced urine output and any seizure or confusion
Reveal answer & rationale
Correct order: B → A → C → D
The blood pressure is the fastest route to harm here — hypertensive emergency with encephalopathy, presenting as seizures and altered consciousness, is a named acute-phase complication — so confirming it and screening for neurologic signs comes first (B). Escalation follows immediately, since the diuretic and any antihypertensive require orders (A). The monitoring and dietary restrictions are nurse-initiated and address the volume problem driving the pressure (C). Family teaching is genuinely essential because most of this treatment happens at home, but it follows stabilization of the immediate concern (D).
Q4 Multiple choice
A 9-year-old presents with cola-coloured urine and periorbital edema. Her mother reports impetigo that resolved about six weeks ago and no recent sore throat. Which statement is most accurate?
  1. A. Six weeks is too long an interval, so post-streptococcal glomerulonephritis is unlikely
  2. B. Post-streptococcal glomerulonephritis follows skin infection at about six weeks, and anti-DNase B rather than ASO is the marker to check
  3. C. This timing indicates IgA nephropathy rather than post-streptococcal disease
  4. D. A normal C3 level would confirm post-streptococcal glomerulonephritis in this case
Reveal answer & rationale
Answer: B
The latency differs by route: about 1 to 3 weeks after pharyngitis but about 6 weeks after a skin infection (impetigo) — so six weeks is exactly the expected interval, not too long (B, refuting A). And because "elevated anti-streptolysin O titers are commonly observed after pharyngitis," anti-DNase B is the marker that matters after impetigo. Option C inverts the timing rule: IgA nephropathy is synpharyngitic, arriving with the infection rather than weeks after it. Option D reverses the complement finding — C3 is low in post-streptococcal disease and returns to normal in 6 to 8 weeks, and a normal complement is one of the three explicit reasons to biopsy.
Q5 Multiple choice
Two days later a different patient with glomerulonephritis reports coughing up blood. Which action is the priority?
  1. A. Document the finding and reassess at the next scheduled observation
  2. B. Escalate immediately — hemoptysis with an active urinary sediment indicates pulmonary-renal syndrome
  3. C. Obtain a sputum culture and start empiric antibiotics for pneumonia
  4. D. Increase the loop diuretic dose, since this represents pulmonary edema from fluid overload
Reveal answer & rationale
Answer: B
The alveolar and glomerular basement membranes share the α-3 chain of type IV collagen, so a single autoantibody attacks both; pulmonary involvement occurs in 40% to 60% of anti-GBM disease and "may be the first clinical feature," with hemoptysis ranging from subtle to life-threatening (B). Option A accepts a delay in a condition that may require mechanical ventilation and plasma exchange. Option C is plausible reasoning that misses the syndrome — note that alveolar hemorrhage on imaging shows bilateral bibasilar opacities where "the apices and costophrenic angles are generally spared." Option D would be reasonable for crackles with rising weight and jugular venous distension, but fluid overload does not cause hemoptysis, and diuresing a patient who is bleeding into their alveoli delays the actual treatment.

Common questions

What causes glomerulonephritis?
Common causes and risk factors include post-streptococcal glomerulonephritis — the most common cause in children worldwide; nephritogenic group a beta-hemolytic streptococci after pharyngitis (about 1–3 weeks) or impetigo (about 6 weeks), other infection-related glomerulonephritis — bacterial (meningococcemia, staphylococcal endocarditis, pneumococcal pneumonia), viral (hepatitis b and c, mumps, hiv, varicella, ebv), parasitic (malaria, toxoplasmosis), iga nephropathy — about 10% of us renal biopsies, up to 40% in east asia; male predominance 2.5:1 in the us and europe; peak incidence in the second and third decades, rapidly progressive disease — pauci-immune (anca-associated) 40–50% of adult cases, immune complex 25–30%, anti-gbm 10–15%, systemic lupus erythematosus and other immune-complex deposition diseases, and others.
What are the early signs of glomerulonephritis?
Early findings include Cola-coloured, tea-coloured or smoky urine — the signature finding.
Which findings should a nurse report immediately in glomerulonephritis?
Report immediately: Hemoptysis or new shortness of breath with an active urinary sediment, Fevers, night sweats, weight loss, arthralgias, oral ulceration, scleritis, epistaxis, sinusitis, palpable purpura, Seizures or altered consciousness with high blood pressure, Generalized muscle weakness or flaccid paralysis, Rapid loss of renal function over days to weeks, and others. These signal deterioration that needs rapid intervention.
What is the difference between nephritic and nephrotic syndrome?
The dividing line is 3.5 g/day of proteinuria. Nephritic syndrome — what glomerulonephritis produces — is hematuria, hypertension, oliguria, and edema with proteinuria in the sub-nephrotic range, under 3.5 g/day. Nephrotic syndrome involves proteinuria exceeding 3.5 g/day. The shorthand: nephritic is blood in the urine with only modest protein; nephrotic is massive protein. Nephritic syndrome is also a syndrome rather than a diagnosis — it "is a common presentation of most proliferative glomerulonephritides," and the job of the workup is to find which one is responsible.
How long after a strep infection does glomerulonephritis appear?
It depends on where the infection was, and this is the detail most commonly taught wrong. After pharyngitis, sources place the interval at 1–2 or 2–3 weeks — so about 1 to 3 weeks after a sore throat. After a skin infection (impetigo), it is about 6 weeks. The serology follows the same split: "elevated anti-streptolysin O titers are commonly observed after pharyngitis," so ASO is the throat marker and anti-DNase B is the one that matters after impetigo. A third pattern rules out both: in IgA nephropathy the hematuria arrives with the infection — synpharyngitic hematuria — rather than weeks later.
Why is a red blood cell cast such an important finding?
Because it localizes the bleeding. "RBC casts are formed when deformed, and distorted RBCs and white blood cells are encased by the Tamm-Horsfall protein," which renal tubular cells secrete normally — so the cast is a mould of the tubule, and the blood must have entered the stream above it, at the glomerulus. That rules out the bladder, the prostate and a stone in one step. Together with dysmorphic red cells and acanthocytes, RBC casts are described as pathognomonic of glomerulonephritis, against a normal upper limit of only 3 RBCs per high-power field.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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