Nephrology
Bootcamp Syllabus

High BUN:Cr, low urine sodium, and a bland sediment mean the tubules are working hard and the problem is upstream: volume and pressure. Rule 1 — localize before you treat. Prerenal fixes with volume; ATN does not; obstruction fixes with a catheter.

Every number in this stem points the same direction. FENa <1%, urine sodium <20 mEq/L, urine osmolality >500, and a BUN:creatinine ratio >20:1 all indicate tubules that are intact and avidly reabsorbing sodium and water in response to reduced perfusion — the definition of prerenal azotemia. A bland sediment confirms the parenchyma is not (yet) injured. The treatment is to restore perfusion with isotonic crystalloid and stop the insult; creatinine should fall within 24–72 hours.

Anuria, suprapubic fullness, BPH, and a new anticholinergic point to acute urinary retention with postrenal AKI. The first step is to confirm and relieve the obstruction — a bedside bladder scan followed by a urethral (or suprapubic) catheter. Creatinine often falls within 24–48 hours. Anticipate post-obstructive diuresis (replace roughly half the output if it exceeds 200 mL/h for 2 hours) and stop the offending drug.

Subacute AKI weeks after a new drug, sterile pyuria with WBC casts, and mild proteinuria is drug-induced acute interstitial nephritis. Proton pump inhibitors are now the most common outpatient cause; β-lactams, NSAIDs, sulfonamides, and checkpoint inhibitors are the others. Stop the drug; give corticosteroids if creatinine does not improve within days.

Loop diuretics force sodium into the urine, so FENa is uninterpretable. FEUrea (<35% prerenal; >50% ATN) is unaffected by diuretics because urea handling is proximal.

The prerenal state has progressed to acute tubular necrosis. There is no drug that reverses ATN; fluids into a patient who is no longer volume-depleted cause pulmonary edema. Management is supportive while the tubules regenerate over 1–3 weeks, with dialysis only for refractory AEIOU indications.

A cylindrical Tamm-Horsfall matrix packed with red cells can only form if red cells entered the tubule from the glomerulus. RBC casts = glomerular bleeding = glomerulonephritis until proven otherwise.

Leukocytes in a cast mean inflammation within the kidney. Sterile pyuria + a new drug = AIN; fever, flank pain, and bacteria = pyelonephritis. Lower urinary tract infection never makes casts.

Sloughed, degenerating tubular epithelial cells form coarse brown granular (“muddy”) casts — the signature of ischemic or toxic ATN. FENa >2% usually accompanies them.

Translucent, empty Tamm-Horsfall protein cylinders. Hyaline casts are normal and increase with dehydration, exercise, diuretics, and prerenal states. They carry no diagnostic weight beyond “the urine is concentrated.”

Lipiduria follows heavy proteinuria: lipid-laden tubular cells (oval fat bodies) and fatty casts that show a Maltese cross under polarized light. This is the urinary signature of nephrotic syndrome.

Square “envelope” crystals are calcium oxalate dihydrate — the most common stone. In a patient with AKI, an anion and osmolar gap, and hypocalcemia, they mean ethylene glycol poisoning (fomepizole + dialysis).

Yellow-brown rhomboids and rosettes in acid urine (pH <5.5). Uric acid stones are invisible on plain X-ray and the only stones that dissolve — potassium citrate to pH 6–6.5.

Coffin-lid prisms of magnesium ammonium phosphate form in alkaline urine (pH >7) made by urease producers (Proteus, Klebsiella, S. saprophyticus). They build staghorn calculi that require complete surgical removal.

Flat, colorless hexagons are pathognomonic of cystinuria (autosomal recessive defect of dibasic amino acid transport) — think of it in a teenager with recurrent stones. Fluids >4 L, alkalinize to pH >7, tiopronin or penicillamine.

Anemia of CKD is a diagnosis of exclusion, and the first thing to exclude — and treat — is iron deficiency. In CKD the thresholds are set higher than in the general population: iron repletion is indicated when TSAT ≤20% and/or ferritin ≤100 ng/mL (≤200 in dialysis patients). Her TSAT of 14% and ferritin of 38 make her iron-deficient. Give iron (oral is reasonable in non-dialysis CKD; IV if oral fails or is not tolerated), then reassess. An ESA is only added if hemoglobin remains <10 g/dL after iron stores are replete, targeting a hemoglobin of 10–11.5 g/dL — never ≥13, because CHOIR, CREATE, and TREAT showed more stroke, thrombosis, and cardiovascular events at higher targets.

This is secondary hyperparathyroidism from CKD-MBD. The sequence is: control phosphate first (diet, then a binder — a non-calcium binder like sevelamer is favored when there is any hypercalcemia or calcification concern), replete nutritional vitamin D if 25-OH D is low, and only then consider active vitamin D or a calcimimetic for persistent PTH elevation. Correcting phosphate alone lowers PTH.

The two discriminators are timing and complement. IgA nephropathy produces synpharyngitic hematuria — gross hematuria 1–3 days into a mucosal infection, often recurrent, with normal C3/C4. It is the most common primary glomerulonephritis worldwide. Post-streptococcal GN, by contrast, is a delayed immune-complex disease appearing 1–3 weeks after pharyngitis (2–6 weeks after impetigo) with low C3. Management of IgAN: RAAS blockade for proteinuria, blood pressure control, and steroids or newer agents (budesonide targeted-release, sparsentan) for persistent proteinuria >0.75–1 g/day; biopsy shows mesangial IgA deposits.

This is anti-GBM (Goodpasture) disease — a pathogenic circulating IgG autoantibody against the α3 chain of type IV collagen that produces linear immunofluorescence and, when the lung is involved, pulmonary hemorrhage (the alveolar basement membrane shares the antigen; smoking and hydrocarbon exposure unmask it). Because the disease is driven by a circulating antibody, plasmapheresis to remove it is the cornerstone of initial therapy, combined with corticosteroids and cyclophosphamide to stop new production. Treatment is urgent: the chance of renal recovery falls sharply once the creatinine exceeds ~5–6 mg/dL or the patient is dialysis-dependent, but plasmapheresis is still indicated for pulmonary hemorrhage regardless of renal prognosis.

Synpharyngitic hematuria (days, not weeks) with normal complement in a young adult is IgA nephropathy. Confirm with biopsy if proteinuria or GFR decline; treat with ACEi/ARB and SGLT2i, steroids or targeted therapy for persistent proteinuria.

Poststreptococcal GN is self-limited in most patients: loop diuretics and antihypertensives for volume and BP, dialysis rarely. Antibiotics do not alter the nephritis (treat any persistent infection). Persistent low C3 beyond 8 weeks or rising creatinine prompts biopsy for MPGN/C3 glomerulopathy or lupus.

Pulmonary-renal syndrome (anti-GBM or ANCA vasculitis) destroys nephrons by the day. Empiric pulse steroids start immediately; plasmapheresis is added for anti-GBM disease, pulmonary hemorrhage, or dialysis-dependent ANCA disease; cyclophosphamide or rituximab follows once the diagnosis is confirmed.

Resistant hypertension with hypokalemia is primary aldosteronism until proven otherwise — the most common secondary cause (5–10% of hypertensives). Screen with the aldosterone/renin ratio; most antihypertensives (except MRAs) can continue for screening; correct potassium first.

A young woman with resistant hypertension, a bruit, hypokalemia (secondary hyperaldosteronism), and beaded mid-distal renal artery disease has fibromuscular dysplasia. Unlike atherosclerotic renal artery stenosis, FMD responds well to balloon angioplasty alone (~85% improved or cured), and stents are avoided because the lesions are non-ostial and stents impair future intervention.

Exercise-associated hyponatremia with seizure is severe symptomatic hyponatremia — the treatment is a 100–150 mL bolus of 3% saline over 10–20 minutes, repeated up to 2–3 times until symptoms improve, aiming for a 4–6 mEq/L rise. The goal is to reverse cerebral edema within the first hour; total correction is then capped at 8 mEq/L per 24 h.

The stepwise algorithm: (1) serum osmolality is low → true hypotonic hyponatremia (not pseudohyponatremia or hyperglycemia); (2) urine osmolality is >100 (here 480) → ADH is acting, so this is not primary polydipsia or low solute intake; (3) volume status is euvolemic and urine sodium is >30–40 → SIADH, once hypothyroidism and adrenal insufficiency are excluded (both done). In a heavy smoker, small cell lung cancer producing ectopic ADH is the diagnosis to chase with a chest CT. Other SIADH causes: CNS disease, pulmonary infection, pain/nausea/post-operative state, and drugs (SSRIs, carbamazepine, cyclophosphamide, NSAIDs, MDMA, antipsychotics). Treatment: fluid restriction (<800–1,000 mL/day), salt tablets, urea, loop diuretic + salt, or tolvaptan for refractory cases; treat the cause.

Hypovolemia with urine Na <20 = appropriate ADH release from volume depletion. Isotonic saline restores volume, switches ADH off, and the kidney excretes the excess water. Check sodium every 4–6 h because the ensuing water diuresis can overshoot.

Urine osmolality <100 means ADH is appropriately suppressed — the kidney is excreting maximally dilute urine and simply cannot keep up with the water load (and low solute intake limits how much water can be excreted). Restrict water, restore solute, and watch for a brisk correction.

A potassium of 7.1 with a widened QRS is minutes from a sine wave and ventricular fibrillation. The first priority is to stabilize the myocardial membrane, and only IV calcium does that: it raises the threshold potential and narrows the QRS within 1–3 minutes, lasting 30–60 minutes. It does not lower the potassium at all — it buys the time for the shifting and removal steps. Calcium is indicated for any ECG change or potassium ≥6.5 mEq/L; repeat the dose if the ECG does not improve in 5–10 minutes. Calcium chloride (three times the elemental calcium) is used through a central line or in arrest. Then: insulin/glucose and albuterol to shift, and a binder, loop diuretic, or dialysis to remove.

Both the ARNI and the MRA reduce mortality in HFrEF; guidelines now favor adding a chronic potassium binder (patiromer or SZC) to keep patients on guideline-directed therapy rather than dropping a life-prolonging drug for a moderate, asymptomatic potassium elevation. Also review diet, supplements, NSAIDs, trimethoprim, and correct any acidosis; loop diuretic uptitration helps if volume allows.

Moderate hyperkalemia without ECG changes and below 6.5 is treated with shift and removal therapy plus close monitoring; calcium is reserved for ECG changes or K ≥6.5. Review the ACEi, diet, and other contributors; a chronic binder lets the ACEi continue.

A wide QRS with absent P waves is one step from a sine wave and arrest. Calcium antagonizes the membrane effect within minutes and is given before anything else — repeated every 5–10 min if the QRS stays wide — then insulin/dextrose and albuterol, then dialysis.

Acidemia with a high PaCO₂ is respiratory acidosis. In acute respiratory acidosis bicarbonate rises only ~1 mEq/L per 10 mmHg rise in PaCO₂ (expected ~26). A bicarbonate of 20 is lower than expected, and the anion gap is 138 − (100 + 20) = 18 with lactate elevation — a concurrent lactic (anion-gap) metabolic acidosis from hypoperfusion/hypoxia. Two primary processes are present.

Chloride-responsive (saline-responsive) metabolic alkalosis: vomiting loses HCl, volume depletion sustains the alkalosis through aldosterone-driven bicarbonate reabsorption and hypokalemia. Urine chloride <20 confirms chloride depletion. Treatment is isotonic saline plus potassium chloride (chloride corrects the alkalosis; potassium must be repleted as chloride) and treating the vomiting.

Flank pain + fever + hydronephrosis behind an obstructing stone = an obstructed, infected kidney, and this patient is already in septic shock. Antibiotics cannot sterilize a closed, pressurized, pus-filled system, so the principle is source control by drainage: a retrograde ureteral stent or a percutaneous nephrostomy tube, whichever is faster and safer at that institution. The AUA 2025 guideline is explicit that this is a urologic emergency and that delaying decompression by ≥2 days increases the odds of death by roughly 29%. Definitive stone treatment is deferred until the infection has been treated (typically 1–2 weeks), because manipulating a stone in an infected system causes life-threatening sepsis.

Recurrent calcium stones with idiopathic hypercalciuria and normal serum calcium/PTH are treated with a thiazide-type diuretic (chlorthalidone, indapamide, HCTZ), which increases distal calcium reabsorption and reduces urinary calcium ~50%, cutting recurrence. Add potassium citrate if hypokalemia or hypocitraturia develops.

Hematuria + proteinuria + sensorineural deafness with an X-linked pattern is Alport syndrome (COL4A5). Early ACEi/ARB therapy, started at the onset of proteinuria (or even earlier in affected males), delays ESKD by years; SGLT2 inhibitors are added. Immunosuppression has no role.

Thick, irregular, enhancing septa without a solid component = Bosniak III (~50% malignant). Management is surgical excision (partial nephrectomy) or ablation, with active surveillance an option in comorbid patients. Bosniak IV (enhancing nodule) is >90% malignant.

BK polyomavirus nephropathy (months 1–12, plasma BK >10,000 copies, SV40-positive biopsy) is managed by reducing immunosuppression; there is no effective antiviral. It mimics rejection clinically and histologically — which is treated by the opposite maneuver.

Fever with rigors during dialysis in a catheter-dependent patient is catheter-related bloodstream infection until proven otherwise; S. aureus (often MRSA) and Gram-negatives predominate. Draw paired cultures, start vancomycin plus an antipseudomonal or third-generation cephalosporin (dosed for dialysis), and remove the catheter when there is hemodynamic instability, S. aureus/Pseudomonas/fungal infection, tunnel infection, or persistent bacteremia; place a temporary catheter and a new tunneled line after clearance. Evaluate for endocarditis and metastatic infection with S. aureus.

Severe-range BP (≥160/110) with headache, thrombocytopenia, and transaminase elevation = preeclampsia with severe features (HELLP spectrum) — proteinuria is not required. Management at ≥34 weeks is magnesium for seizure prophylaxis, IV antihypertensives within 30–60 min, and delivery.

AKI + anemia + hypercalcemia + bone pain + low anion gap + dipstick-negative but UPCR-positive proteinuria = multiple myeloma with light-chain (cast) nephropathy. The dipstick detects only albumin. Serum free light chains and SPEP/UPEP with immunofixation establish the diagnosis; treatment is urgent bortezomib-based therapy plus hydration.

SGLT2 inhibitors cause euglycemic diabetic ketoacidosis under fasting, surgical stress, and dehydration; the FDA recommends holding them 3–4 days before scheduled surgery (ertugliflozin 4 days) and resuming once eating normally. Also hold on sick days (SADMANS).

Lithium enters principal cells through ENaC and blocks ADH signaling, causing nephrogenic diabetes insipidus. Amiloride blocks ENaC, reduces lithium entry, and improves the concentrating defect while allowing lithium to continue. Ensure free water access and monitor lithium levels and creatinine.

Missed dialysis + bradycardia + wide QRS + absent P waves is hyperkalemia until proven otherwise. Calcium first, before the potassium result; pacing and atropine fail because the myocardium cannot conduct.

Free-water overload during endurance exercise causes acute hyponatremic cerebral edema. A seizing patient gets a hypertonic bolus immediately; check the sodium but do not wait for it.

An infected system under pressure is urosepsis that antibiotics cannot reach. Decompress today; treat the stone after the infection clears.

Anti-GBM disease or ANCA vasculitis. Serologies and biopsy are sent, but steroids start now; plasmapheresis follows for pulmonary hemorrhage or anti-GBM.

Encephalopathy and papilledema define emergency; the MAHA is hypertension-driven and resolves with controlled BP reduction.

Symptomatic hypocalcemia (tetany) and severe hyperkalemia justify calcium now despite the calcium-phosphate product; then rasburicase, fluids, and early dialysis for refractory electrolytes.

Pigment nephropathy: the dipstick sees myoglobin, the microscope sees no cells. Early aggressive isotonic fluid is the only intervention that changes the renal outcome; manage the potassium in parallel.

Uremic pericarditis is a dialysis indication; heparin-free runs reduce the risk of hemorrhagic effusion and tamponade. Serial echocardiography for effusion size.

Na ≤105, alcohol use, hypokalemia, and liver disease are every risk factor for osmotic demyelination. Lethargy without seizure is not an indication for rapid correction; the goal is a slow, controlled rise.

Rigors with fever in a catheter-dependent patient is line sepsis; hypotension mandates catheter removal, not salvage. S. aureus is the leading organism.

Synpharyngitic hematuria with normal complement is IgA nephropathy; PSGN follows by 1–3 weeks with low C3.

Inability to acidify urine below 5.5 with hypokalemia and stones is distal RTA; Sjögren is a classic cause.

Myoglobinuria. Aggressive isotonic crystalloid to high urine output.

Urine osmolality <100 means ADH is suppressed; the kidney cannot excrete water without solute. Risk of brisk overcorrection once solute is given.

ECG changes mandate membrane stabilization before anything else.

Membranous nephropathy carries the highest thrombosis risk; renal vein thrombosis presents with flank pain, hematuria, and AKI. Anticoagulate.

FMD responds to angioplasty alone; stents are avoided.

SGLT2 inhibitors are initiated down to eGFR 20; potassium 5.2 is managed to keep the ARB.

Oxalate crystals, hypocalcemia, and AKI with a dual gap = ethylene glycol; fomepizole plus dialysis.

β₂-microglobulin is not cleared by conventional dialysis and deposits in joints and carpal tunnel after years.

Pregnancy is one of two indications to treat ASB; untreated, 20–30% progress to pyelonephritis.

CMV disease peaks at 1–6 months: fever, leukopenia, colitis, hepatitis. Treat with (val)ganciclovir; prophylaxis in D+/R−.

This is cardiorenal syndrome with venous congestion. Renal function improves with decongestion, not with fluids or diuretic withdrawal; a modest creatinine rise during effective diuresis does not worsen outcomes (DOSE, CARRESS-HF). Escalate the loop and add sequential blockade; GDMT continues if potassium and BP allow.

Nephritic-nephrotic overlap with hypocomplementemia in lupus is proliferative (class III/IV ± V) nephritis until biopsied. Biopsy defines class; induction is steroids plus MMF or low-dose cyclophosphamide, with belimumab or voclosporin added per 2024 KDIGO/ACR guidance, ACEi/ARB for proteinuria and BP, and hydroxychloroquine continued for all.

Thiazides raise uric acid and lower potassium; in a patient with gout and CKD they are a poor fit. Amlodipine or maximizing RAAS blockade avoids both problems, and losartan is uniquely uricosuric among ARBs.

Total-body potassium is depleted in DKA; insulin drives the remainder into cells and can cause fatal hypokalemia. Replace potassium to ≥3.3 before insulin. The creatinine reflects prerenal AKI that improves with fluids.

Delayed, stepwise creatinine rise after arterial instrumentation with livedo, eosinophilia, and a bland sediment is cholesterol (atheroembolic) disease. There is no specific therapy; supportive care, statins, and avoidance of further catheterization or intensification of anticoagulation are the management.

Missed dialysis + wide QRS without P waves = hyperkalemia. Calcium restores membrane excitability in minutes.

Uncomplicated stones ≤10 mm are managed expectantly; tamsulosin improves passage of distal stones 5–10 mm; follow-up imaging at 2 weeks confirms passage.

Gap acidosis (AG 30) plus an osmolar gap (44) with oxalate crystalluria and hypocalcemia is ethylene glycol poisoning. Fomepizole blocks metabolism; dialysis removes the parent alcohol and metabolites when acidosis or AKI is present.

An SGLT2 inhibitor is the second pillar for albuminuric CKD (eGFR ≥20), independent of glycemic effect. Finerenone or a GLP-1 RA would be subsequent additions.

Isolated familial microhematuria with normal function, no proteinuria, and no hearing/eye disease is thin basement membrane disease — benign and monitored, not investigated invasively.

Seizure from hyponatremia is severe symptomatic hyponatremia regardless of cause; a hypertonic bolus is given immediately. Because psychogenic polydipsia auto-corrects rapidly once water stops, cap the 24-h rise at 8 mEq/L afterward and be ready with D5W/desmopressin.

Macrolides inhibit CYP3A4 and raise tacrolimus levels; tremor, hyperkalemia, and a reversible creatinine rise are the classic toxicity triad. Check the trough and reduce the dose or change the antibiotic.

An infected system behind an obstructing stone is a closed-space abscess; antibiotics cannot sterilize it. Decompress the same day; definitive stone treatment comes after sepsis resolves.

The NSAID (afferent constriction) + ACEi (efferent dilation) + diuretic (volume depletion) “triple whammy” is the most common outpatient prerenal AKI. Remove the offenders and restore volume; expect recovery within days.

Nephrotic children lose IgG and complement factors in the urine and have ascites — the classic infectious complication is primary peritonitis with Streptococcus pneumoniae. Paracentesis and ceftriaxone.

Loss of thrill/bruit = access thrombosis. Salvage rates fall with every hour; same-day thrombectomy (surgical or endovascular) with treatment of the underlying stenosis preserves the access.

Hypomagnesemia causes renal potassium wasting through ROMK channels; potassium cannot be repleted until magnesium is corrected.

Hypertension with unprovoked hypokalemia and metabolic alkalosis is primary aldosteronism until proven otherwise; the aldosterone/renin ratio is the screen (ACEi/CCB can continue for screening; MRAs must be stopped).

Nitrofurantoin requires adequate urinary concentration to work and accumulates systemically at reduced GFR, causing pulmonary toxicity and neuropathy; most guidelines avoid it below CrCl 30 and use caution at 30–45.

Upper airway disease + pulmonary hemorrhage + pauci-immune GN + purpura in an older adult with normal complement is granulomatosis with polyangiitis; c-ANCA/PR3 is positive in ~90% of generalized disease. Biopsy confirms; rituximab or cyclophosphamide with steroids.

Tumor lysis syndrome with AKI and refractory electrolytes needs rasburicase (degrades existing urate), volume, hyperkalemia therapy, and dialysis when electrolytes are refractory. Calcium is normally withheld because of calcium-phosphate precipitation — but tetany and severe hyperkalemia make it necessary here.

The vancomycin + piperacillin-tazobactam combination and a high trough are the tested nephrotoxic pairing. Remove the offenders, re-dose vancomycin by AUC if still required, and support.

Hypertension after 20 weeks with thrombocytopenia and transaminitis is preeclampsia with severe features (HELLP spectrum) even without proteinuria. Magnesium, BP control, corticosteroids for fetal lung maturity at <34 weeks, and delivery.

The heme reagent reacts with myoglobin and hemoglobin as well as red cells. A positive dipstick with no RBCs on microscopy plus a CK >5× normal is myoglobinuria; treat with aggressive isotonic fluids.

PaCO₂ is 26 above 40; chronic compensation raises HCO₃ by ~3.5 per 10 (expected ~33–35), which matches. The near-normal pH reflects full renal compensation, not a second disorder.

Iron deficiency (TSAT ≤20%, ferritin ≤100) must be corrected before an ESA; many patients respond to iron alone, and ESAs given to iron-deficient patients are ineffective and raise thrombotic risk.

Membranous nephropathy carries the highest risk of renal vein thrombosis, especially with albumin <2.5; flank pain, hematuria, and AKI are the triad. Confirm with CT/MR venography and anticoagulate.

PD peritonitis is treated empirically with intraperitoneal antibiotics covering Gram-positive and Gram-negative organisms; the catheter stays unless the infection is fungal, refractory beyond 5 days, relapsing, or associated with tunnel infection.

Concentrated urine means the kidney is responding to ADH normally — this is a water deficit from impaired access and thirst. Replace free water slowly; rapid correction causes cerebral edema.

The IDEAL trial showed no benefit to starting dialysis early based on eGFR alone; initiation is driven by symptoms and refractory metabolic complications. He should already be listed for transplant and continue fistula maturation.