Renal question bank

B. Bicarbonate wasting from blocked proximal-tubule carbonic anhydrase, with chloride retained in its place — Acetazolamide blocks luminal and cellular carbonic anhydrase in the proximal tubule, so filtered bicarbonate is lost (bicarbonaturia) and the urine is alkaline; serum HCO₃⁻ falls and chloride replaces the lost negative charge, giving a normal anion gap (here 10), hyperchloremic metabolic acidosis. Acetazolamide is not metabolized, so there is no unmeasured acid. Losing sodium-rich, bicarbonate-poor fluid causes a contraction alkalosis — the loop diuretics’ pattern — which would raise, not lower, the bicarbonate. Hyperventilation is the compensation for the acidosis, not its cause.

D. The falling serum bicarbonate leaves less substrate for carbonic anhydrase–dependent reabsorption, and distal segments reclaim the extra sodium — As bicarbonaturia lowers serum bicarbonate, less substrate is available for carbonic anhydrase–mediated sodium reabsorption, so acetazolamide becomes less efficient; the loop, distal tubule and ENaC-bearing nephron also reabsorb the extra sodium delivered to them. Acetazolamide is not metabolized, so it does not induce its own metabolism, and protein-bound diuretics reach the lumen by tubular secretion rather than filtration. A higher dose would not help: the label notes that increasing the dose does not increase the diuresis, and it gives edema doses intermittently so the kidney can recover.

E. Mannitol has shifted water from the cells into the plasma, expanding the circulation before the diuresis — Mannitol raises plasma osmolality and draws water out of the cells into the plasma, increasing blood volume before the kidneys excrete it; overt expansion of extracellular volume can precipitate pulmonary edema in heart failure, and severe pulmonary vascular congestion or edema contraindicates it. Entry into the brain worsens cerebral edema rather than the lungs. Anaphylaxis would bring hypotension and other allergic signs, hypokalemia does not cause crackles, and mannitol does not inhibit carbonic anhydrase.

C. Urinary alkalinization that increases tubular ammonia reabsorption — Urinary alkalinization increases the renal tubular reabsorption of ammonia, and acetazolamide decreases ammonia clearance, so it may precipitate hepatic encephalopathy — which is why both CAIs are contraindicated in cirrhosis. CAIs increase potassium excretion rather than retaining it, and in hepatic insufficiency that potassium loss could itself precipitate hepatic coma. They waste bicarbonate and cause a hyperchloremic metabolic acidosis, not an alkalosis, and the osmotic plasma expansion belongs to mannitol, not to a carbonic anhydrase inhibitor.

B. It must be secreted into the proximal tubule to act and is cleared by the kidney, so poor renal function blunts its effect and favors metabolic acidosis — Acetazolamide reaches its luminal target by secretion through the proximal tubule’s organic anion transporters; almost 90% is excreted by tubular secretion, and it is ineffective in renal insufficiency. Marked kidney disease is a labeled contraindication, and metabolic acidosis can be severe when renal function is reduced. It is not metabolized (so not a prodrug), it causes hypokalemia rather than hyperkalemia, filtration without reabsorption describes mannitol, and despite its protein binding acetazolamide is dialyzable.

E. Gs activation, a rise in cAMP and insertion of aquaporin-2 into the apical membrane — He has central DI: water deprivation failed to concentrate the urine, and desmopressin, a selective V2 agonist, raised urine osmolality. V2 is Gs-coupled; cAMP activates protein kinase A, which inserts aquaporin-2 into the apical membrane. Gq–IP3 signaling is the V1 vascular pathway, and V2 blockade is the action of the vasopressin antagonists. Thiazides act on the Na⁺–Cl⁻ cotransporter, and ENaC is a sodium channel — the route by which lithium enters principal cells — whereas water crosses through aquaporin-2.

A. Lithium entering principal cells through ENaC and disrupting aquaporin-2 — No response to desmopressin means nephrogenic DI. About 20% of patients on chronic lithium develop it: lithium enters collecting-duct principal cells through ENaC and disrupts aquaporin-2. Failure of ADH secretion is central DI, which would respond to desmopressin, and excess ADH (SIADH) causes water retention, not polyuria. In primary polydipsia the urine concentrates during water deprivation, which hers did not.

C. It triggers exocytosis of von Willebrand factor and factor VIII from endothelial Weibel-Palade bodies — The cAMP signaling that desmopressin triggers also releases stored von Willebrand factor and factor VIII, including from Weibel-Palade bodies; factor VIII rises within 30 minutes. It is a synthetic vasopressin analog, not a factor concentrate, and it has little V1 vasopressor activity. Rather than inhibiting fibrinolysis, desmopressin raises plasminogen activator along with factor VIII. In type 2B disease the same release can cause thrombocytopenia.

D. Water retention lowering extracellular osmolarity, so water enters and swells neurons — Desmopressin keeps the kidney retaining water while he continues to drink — an SIADH-like state — so serum sodium falls; as extracellular osmolarity drops, water moves into neurons and the swelling causes confusion, seizures and coma. Older age raises the risk. Desmopressin has little V1 vasopressor activity, hypernatremia is the picture of untreated DI, and osmotic demyelination is a complication of correcting hyponatremia too fast, not of the hyponatremia itself.

B. Reversible diabetes insipidus after vasopressin withdrawal — The vasopressin label warns of reversible diabetes insipidus — polyuria, dilute urine and hypernatremia — after the infusion is stopped; urine output, fluid status and electrolytes are monitored, and some patients need vasopressin again or desmopressin. SIADH would retain water and lower sodium. After the infusion is stopped, vasopressin’s pressor effect simply fades within 20 minutes, and vasoconstriction would not explain a dilute polyuria with a rising sodium. Primary polydipsia gives a normal or low plasma osmolality, not a rising sodium.

D. More free water excreted, with sodium excretion largely unchanged — Tolvaptan blocks the V2 receptor, so aquaporin-2 is not inserted and free-water clearance rises (aquaresis) while urine osmolality falls. Urinary sodium and potassium excretion are not significantly changed. Less urine with a higher osmolality is what V2 stimulation does (the desmopressin effect), and glucose in the urine is the signature of SGLT2 inhibitors.

A. Injury to brain cells adapted to chronic hypotonicity after a rapid rise in sodium — Within about 48 hours the brain adapts to hyponatremia; raising sodium too quickly then causes osmotic demyelination, with dysarthria, dysphagia and quadriparesis typically delayed by a few days, and malnutrition and alcohol use raise the risk. Water moving into neurons (cerebral edema) is the mechanism of falling sodium, whereas hers rose; cerebral salt wasting and ectopic vasopressin are causes of hyponatremia, not of a rising sodium. Liver injury presents with fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice rather than this delayed bulbar and limb weakness.

E. Stop tolvaptan, repeat liver tests within 48–72 hours, and do not restart — Jynarque carries a boxed warning for serious liver injury. If ALT, AST or bilirubin rises above 2 times normal it is stopped immediately and tests are repeated within 48 to 72 hours; it is not restarted in a patient whose ALT or AST ever exceeded 3 times normal unless another cause is found and the injury has resolved. Samsca is the same drug and is not used for ADPKD outside the REMS, and a CYP3A inhibitor would raise tolvaptan exposure.

C. It removes free water from a patient who is already volume-depleted — Hypovolemic hyponatremia is a labeled contraindication: tolvaptan’s aquaresis removes free water, deepening the volume loss; such patients are treated with isotonic fluid. Tolvaptan does not cause natriuresis — urinary sodium excretion is not significantly changed — and it is V2-selective (29 times its V1a affinity). Hypovolemia stimulates vasopressin release rather than suppressing it, and tolvaptan is cleared almost entirely by CYP3A, with less than 1% excreted unchanged in urine.

C. Intravenous calcium gluconate — With hyperkalemia changing the ECG, calcium is given first: it stabilizes cardiac membranes and is first-line for cardiac toxicity, although it does not lower potassium. The other options act on the potassium itself — insulin and albuterol shift it into cells, bicarbonate helps when there is metabolic acidosis, and cation exchangers remove it — and dialysis is the definitive treatment in end-stage kidney disease.

D. Replace magnesium — Low magnesium increases urinary potassium loss through ROMK channels and lowers intracellular potassium, so potassium replacement alone may fail; magnesium is replaced first. Infusing potassium rapidly can cause cardiac arrest, dextrose stimulates insulin and drives potassium into cells (as would an insulin infusion), and diuretics promote urinary potassium excretion.

E. Loss of the patellar reflex — Deep tendon reflexes decrease once magnesium rises above about 4 mEq/L and disappear as it approaches 10 mEq/L, where respiratory paralysis may follow; disappearance of the patellar reflex is the useful clinical sign of onset, which is why the knee jerk is checked before each dose. Respiratory paralysis comes later, peaked T waves are hyperkalemia, U waves are hypokalemia, and a Chvostek sign reflects hypocalcemia.

A. Citrate in the stored blood binds circulating calcium — Citrate, the anticoagulant in stored blood, binds circulating calcium and lowers the ionized fraction acutely after massive transfusion. Acidosis does the opposite — it reduces albumin binding and raises ionized calcium. Hypoalbuminemia lowers total calcium while ionized calcium stays normal, the reverse of this picture, and parathyroid hormone and activated vitamin D raise serum calcium.

C. Its onset of action is delayed — Binders lower potassium only as it is bound in the gut and excreted, so the fall takes hours: the patiromer and SZC labels exclude emergency use for that reason, and SPS may take hours to days. They do not block renal secretion; they raise fecal potassium excretion, and urinary potassium excretion falls. They are not contraindicated in kidney disease (93% of the adults in patiromer’s trials had chronic kidney disease), they act by binding potassium in the gut rather than through a shift into cells, and none of them is absorbed.

D. Intestinal necrosis — Intestinal necrosis, with bleeding, ischemic colitis or perforation, has been reported with SPS, mostly when sorbitol was given at the same time, and recent intestinal surgery is a risk factor. SPS is avoided in patients who have not had a bowel movement after surgery. SPS removes magnesium (hypomagnesemia, not hypermagnesemia). Aspiration causes bronchitis or bronchopneumonia, not GI bleeding. Systemic alkalosis follows co-administration with magnesium hydroxide or aluminum carbonate, and the sodium load causes fluid retention, not bloody stools.

A. Patiromer binds magnesium in the colon — Patiromer binds magnesium in the colon, which can cause hypomagnesemia (an adverse reaction in 5.3% of adults); serum magnesium is monitored and supplemented if it falls. Raising gastric pH is SZC’s effect, not patiromer’s. Patiromer is not absorbed, so it acts in the gut lumen, not the renal tubule. Her potassium is normal, so hyperkalemia is not the cause, and the small change in serum bicarbonate on the labels is a rise, seen with SZC.

E. It contains sodium — SZC contains sodium, and in trials edema rose with dose. Its label advises watching for edema in patients prone to fluid overload, such as those with heart failure or kidney disease, adjusting dietary sodium and increasing diuretics as needed. Binding magnesium in the colon is patiromer’s effect. SZC captures potassium in exchange for hydrogen and sodium, not calcium, and it raises serum bicarbonate slightly rather than lowering it. It is not absorbed (zirconium levels were similar in treated and untreated patients), so it cannot act on the collecting duct.

B. A thiazide, which blocks NCC in the distal convoluted tubule — Thiazides block NCC and reduce urinary calcium by up to 50%: calcium is retained proximally after volume depletion and possibly distally. Loops do the opposite — blocking NKCC2 removes the lumen-positive voltage that drives paracellular calcium reabsorption, causing calciuria. Aldosterone antagonists act on the collecting duct and mainly spare potassium. Acetazolamide alkalinizes the urine, which favors kidney stones rather than protecting against calcium loss, and mannitol is an IV osmotic agent for raised intracranial or intraocular pressure, not a long-term antihypertensive.

E. Amiloride — Amiloride blocks ENaC in the late distal tubule and collecting duct, so less potassium and H⁺ are secreted, and it decreases the magnesium loss caused by thiazides and loops; ENaC blockers are used to correct diuretic hypokalemia and hypomagnesemia. Bumetanide is another loop diuretic and metolazone another thiazide-like drug, which would add to the losses; acetazolamide causes hypokalemia, and mannitol causes electrolyte losses of its own.

D. Tolvaptan — Tolvaptan blocks the V2 receptor, so aquaporin-2 is not inserted: urine water excretion and free-water clearance rise and serum sodium increases, while urinary sodium and potassium excretion are not significantly changed; it is used for hypervolemic and euvolemic hyponatremia such as heart failure. Furosemide and hydrochlorothiazide are natriuretic and cause hypokalemia — thiazides are a common cause of hyponatremia — spironolactone retains potassium, and acetazolamide causes bicarbonate loss.

A. Acetazolamide — Acetazolamide blocks proximal-tubule carbonic anhydrase, so bicarbonate is lost in the urine and serum bicarbonate falls — the logic behind its use to reverse metabolic alkalosis — and it also overcomes proximal reabsorption when a loop diuretic is not enough. A thiazide, like the loop, sends more sodium to the collecting duct and causes metabolic alkalosis. Mannitol expands the circulation before it is excreted and can precipitate pulmonary edema in heart failure, and tolvaptan removes free water without significantly changing urinary sodium or potassium excretion.

C. It produces a nephrogenic, dose-dependent resistance to ADH — a reversible DI-like state — Demeclocycline, a tetracycline, can cause a diabetes insipidus syndrome that is nephrogenic, dose-dependent and reversible on stopping; that is why it is effective in SIADH, although it is nephrotoxic and used only when other therapies fail. Dual V1A/V2 blockade describes conivaptan, and V2 stimulation is desmopressin, which would worsen hyponatremia. Blocking NCC (a thiazide) is a common cause of hyponatremia, and ENaC blockade is amiloride’s action. Tolvaptan is avoided in underlying liver disease.

A. Inappropriately high ADH action retaining free water (SIADH) — She meets the SIADH pattern — low serum osmolality, urine osmolality above 100 mOsm/kg and urine sodium above 40 mEq/L, no volume depletion, with hypothyroidism and adrenal insufficiency excluded — and carbamazepine is one of the drugs that cause it. Renal resistance to ADH is nephrogenic DI, which causes dilute urine and hypernatremia. She takes no thiazide, and hypovolemic hyponatremia requires volume depletion.

D. Mild volume depletion increases proximal sodium and water reabsorption, so less urine is made — Thiazides block NCC; the increased distal sodium excretion and mild volume depletion trigger compensatory proximal reabsorption of sodium and water, which impairs the kidney’s maximum diluting capacity and decreases urine production. They do not act on the V2 receptor, and in nephrogenic DI ADH secretion is already normal — the defect is in the kidney’s response. Blocking ENaC is amiloride’s action; lithium enters principal cells through ENaC, and amiloride may help lithium-induced polyuria.

E. Insulin drives potassium into cells, unmasking a total body deficit — Insulin deficiency in diabetic ketoacidosis shifts potassium out of cells, so serum potassium can be high even though total body potassium is depleted; insulin then promotes cellular potassium uptake, and the deficit appears. Insulin moves potassium into cells rather than out in the urine. Blocking ENaC or lowering aldosterone would reduce potassium secretion and raise serum potassium, as potassium-sparing diuretics and ACE inhibitors do.

B. Both reduce aldosterone’s drive for distal potassium secretion — Lisinopril removes the angiotensin II that drives aldosterone secretion, and spironolactone blocks aldosterone’s mineralocorticoid receptor, suppressing the aldosterone-induced proteins that raise ENaC activity — either way less potassium is secreted. Her diabetes, kidney disease and NSAID add to the risk. More distal sodium delivery is how loops and thiazides lower potassium; amiloride and triamterene are the drugs that block ENaC directly; alkalemia moves potassium into cells, and potassium-sparing diuretics cause a hyperchloremic acidosis; NKCC2 is the loop-diuretic target.

D. β-adrenergic stimulation shifting potassium into cells — β-adrenergic stimulation promotes cellular potassium uptake, so inhaled β-agonists lower serum potassium by redistribution rather than loss — which is why rebound hyperkalemia can follow repletion once the shift resolves. Increased distal sodium delivery is the diuretic mechanism, and aldosterone-driven secretion goes with it; he has no gastrointestinal losses, and his normal magnesium rules out ROMK inhibition from hypomagnesemia.

C. Diluted IV potassium chloride in saline, guided by the ECG — IV repletion is preferred with dysrhythmias and digitalis toxicity, the potassium chloride must be diluted, and therapy is guided by serial ECGs, especially with digitalis. Direct injection of the concentrate may be instantaneously fatal. Dextrose stimulates insulin and drives potassium into cells, so saline is the vehicle. Oral replacement alone ignores the indication for IV therapy here, and sodium polystyrene sulfonate removes potassium.

E. Reduced glomerular filtration from the combined hemodynamic effects of her drugs — NSAIDs inhibit the renal prostaglandins that dilate the afferent arteriole, ACE inhibitors remove the efferent arteriolar tone that maintains filtration, and the “triple whammy” of an ACE inhibitor or ARB, a diuretic and an NSAID increases the risk of acute kidney injury; hyperkalemia can occur with NSAIDs. Crystal nephropathy comes from poorly soluble drugs such as acyclovir, ampicillin and sulfonamides, and direct proximal tubular toxicity from drugs such as aminoglycosides, amphotericin B and cisplatin. Nephrogenic diabetes insipidus is lithium’s effect, and rhabdomyolysis is excluded by a normal creatine kinase.

C. The proximal tubular cells, where it accumulates — Gentamicin accumulates in renal proximal tubular cells and damages them; nephrotoxicity appears in up to 10 to 25% of patients, is generally reversible, and is more likely with high or prolonged dosing. The label calls for examining the urine for decreased specific gravity, protein, cells or casts and for periodic BUN and creatinine. Blocking afferent dilation is the NSAID mechanism, a hypersensitivity interstitial nephritis is typical of β-lactams and NSAIDs, and a reduced response to ADH in the collecting duct is lithium’s nephrogenic diabetes insipidus.

A. Stop the nafcillin — Nafcillin is associated with renal tubular damage and interstitial nephritis, presenting with hematuria, proteinuria and acute kidney injury that may come with rash, fever and eosinophilia; most cases resolve when it is stopped, and withdrawing the offending drug is the mainstay of treatment. Corticosteroids are considered only if renal function has not improved 5 to 7 days after the drug is withdrawn. Ampicillin is another β-lactam — the class most likely to cause this hypersensitivity picture — and fever, rash and eosinophilia point to interstitial nephritis, not a prerenal cause.

B. Nephrogenic systemic fibrosis — Nephrogenic systemic fibrosis is a progressive multiorgan fibrosing condition caused by gadolinium-based contrast agents in the setting of low GFR, usually stage 4 or 5 chronic kidney disease; linear agents bind gadolinium less tightly and carry more risk, and the FDA placed a boxed warning on gadolinium products in severely decreased GFR. A creatinine rise within 24 hours that peaks at 3 to 5 days is contrast-induced nephropathy from iodinated contrast. Interstitial nephritis is typical of NSAIDs and antibiotics, and crystal nephropathy of poorly soluble drugs such as acyclovir.

A. Hypertonic (3%) saline — Severe symptoms such as seizures need urgent initial correction with hypertonic saline, given with careful monitoring and strict limits on the rate of sodium correction to prevent osmotic demyelination. Tolvaptan should not be used when sodium must be raised urgently to prevent or treat serious neurologic symptoms. Desmopressin concentrates the urine and can itself cause hyponatremia, and 5% dextrose acts as free water once the dextrose is metabolized, letting water shift into cells.

C. Tolvaptan acutely reduces extracellular fluid volume, which can raise serum potassium — Tolvaptan acutely reduces extracellular fluid volume, which can raise serum potassium, and hyperkalemia was reported more often when it was given with ACE inhibitors, angiotensin receptor blockers or potassium-sparing diuretics. Both of his other drugs already limit potassium secretion: lisinopril by lowering aldosterone, and spironolactone by blocking its receptor. Tolvaptan itself is a selective V2-receptor antagonist that does not change urinary potassium excretion significantly; ENaC is the target of amiloride.

A. Empagliflozin — An SGLT2 inhibitor used with lithium may decrease serum lithium concentrations, so lithium is monitored more often when empagliflozin or dapagliflozin is started. Diuretics do the opposite: they reduce the renal clearance of lithium and add a high risk of lithium toxicity, and thiazides in particular increase lithium reabsorption in the proximal tubule.

B. Eplerenone — Primary aldosteronism — autonomous aldosterone production from an adenoma or bilateral adrenal hyperplasia, with suppressed renin and often hypokalemia — is managed medically with mineralocorticoid-receptor antagonists, and eplerenone is favored for its selective mineralocorticoid antagonism. A thiazide or a loop diuretic sends more sodium to the aldosterone-sensitive collecting duct and increases potassium and hydrogen excretion, deepening the hypokalemia, and acetazolamide also causes hypokalemia through increased distal sodium delivery.

E. Furosemide — Loop diuretics, with salt tablets, are a second-line therapy that lowers urine concentration in SIADH, whose mainstay is water restriction: blocking NKCC2 reduces interstitial tonicity, so the countercurrent concentrating mechanism fails and free-water excretion rises. Thiazides leave the concentrating mechanism intact and reduce free-water clearance, which is why hyponatremia most often results from them. Hyponatremia is also an adverse effect of spironolactone and of acetazolamide, and mannitol draws water from the cells into the plasma, causing dilutional hyponatremia.

B. Mannitol has drawn water from the cells into the plasma, diluting the sodium — Mannitol raises serum osmolality and shifts water from the intracellular compartment into the plasma, which can cause dilutional hyponatremia; serum osmolarity and the osmol gap are monitored during treatment. SIADH requires a serum osmolality below 275 mOsm/kg, and primary polydipsia has a normal or low plasma osmolality, whereas hers is high. Osmotic diuretics do not interfere with electrolyte reabsorptive mechanisms; NKCC2 is the target of the loop diuretics.

C. Intravascular volume loss from empagliflozin’s glucose-driven diuresis on top of the loop diuretic — Empagliflozin can cause intravascular volume depletion, with symptomatic hypotension or acute changes in creatinine; elderly patients and those on loop diuretics are at higher risk, and given with diuretics it increases urine volume. Volume depletion is corrected before it is started. The hypoglycemia risk of SGLT2 inhibitors comes with insulin or an insulin secretagogue, and his glucose is normal; euglycemic ketoacidosis requires a severe metabolic acidosis, with a bicarbonate below 18 mEq/L. Empagliflozin inhibits SGLT2 in the proximal tubule, not NKCC2.

E. Desmopressin — In chronic hyponatremia the brain has adapted, so rapid correction risks osmotic demyelination; desmopressin or free water can be given if correction is too rapid, and desmopressin is also started alongside 3% saline to prevent overly rapid correction. Desmopressin acts at the V2 receptor to decrease urine volume and increase urine osmolality. Tolvaptan increases free-water clearance and a loop diuretic increases free-water excretion, so both would raise her sodium further; mannitol’s osmotic diuresis can cause hypernatremia; and hypertonic saline is the treatment for severe symptomatic hyponatremia, not a brake on correction.

D. More sodium reaches the macula densa, and tubuloglomerular feedback constricts the afferent arteriole — SGLT2 inhibitors reduce sodium reabsorption and increase sodium delivery to the distal tubule. When the macula densa senses more NaCl, tubuloglomerular feedback constricts the afferent arteriole; the lower intraglomerular pressure decreases albuminuria and slows CKD progression. ACE inhibition is her lisinopril’s action: it reduces constriction of the efferent arterioles, lowering intraglomerular pressure and proteinuria. NKCC2 in the thick ascending limb is the target of loop diuretics, and ENaC is blocked by amiloride.

A. Acetazolamide may worsen her metabolic acidosis, and salicylate raises free acetazolamide levels — Acetazolamide should not be used to alkalinize the urine after a salicylate overdose because it may worsen metabolic acidosis: its bicarbonaturia lowers serum bicarbonate, causing a hyperchloremic metabolic acidosis. Salicylates also displace acetazolamide from plasma protein and inhibit its renal clearance, raising free acetazolamide and causing toxicity through red-cell carbonic anhydrase inhibition. The alkaline urine itself is real — renal bicarbonate loss alkalinizes the urine — but as serum bicarbonate falls, less substrate is left for carbonic anhydrase and the diuresis weakens rather than strengthens; renal excretion is its primary route of elimination, and an IV form is available. Forced alkaline diuresis for salicylate poisoning pairs urinary alkalinization with a loop diuretic.

D. Severe hyponatremia as she keeps drinking while her urine is concentrated — A urine osmolality above 750 mOsm/kg during water deprivation, with a normal or low plasma osmolality, points to primary polydipsia: she releases ADH normally. Severe hyponatremia can occur if primary polydipsia is misdiagnosed as diabetes insipidus and desmopressin is started, because desmopressin decreases urine volume and increases urine osmolality while her high fluid intake continues. Kidneys that do not respond to ADH would not concentrate during water deprivation (nephrogenic DI), and antidiuretic doses of desmopressin are usually below the threshold for effects on vascular smooth muscle.

B. Hypertonic (3%) saline — Hypertonic saline is also used to treat high intracranial pressure but is not a diuretic; it draws water from the intracellular compartment into the extracellular space. Mannitol is contraindicated in anuria: it accumulates when renal excretion is insufficient, and a patient who becomes anuric while receiving it is at risk of heart failure, pulmonary edema, hypertensive crisis, coma and death. Lactated Ringer’s is isotonic and stays in the extracellular compartment without drawing water out of cells, and 5% dextrose acts as free water, letting water shift into cells.