Nephrology

01 Renal Anatomy & Nephron Physiology

Nephrology is the medical specialty devoted to the kidneys — a pair of retroperitoneal, bean-shaped organs that filter roughly 180 liters of plasma per day, adjust salt and water balance, excrete nitrogenous waste, regulate acid-base status, control blood pressure through the renin-angiotensin-aldosterone system (RAAS), activate vitamin D, and stimulate red-cell production via erythropoietin. A scribe who does not understand the nephron will never write a convincing nephrology note, because virtually every diagnosis in this field is a story about one or more segments of the nephron failing to do their job.

Gross Anatomy

Each kidney sits at the T12–L3 level, surrounded by Gerota's fascia and perirenal fat. The outer cortex contains glomeruli, proximal and distal convoluted tubules, and cortical collecting ducts. The inner medulla is organized into pyramids whose apices (papillae) empty into minor calyces, which merge into major calyces, then the renal pelvis, then the ureter. Blood enters via the renal artery (a direct branch of the abdominal aorta just below the SMA at L1–L2), which divides into segmental, interlobar, arcuate, interlobular, and finally afferent arterioles supplying each glomerulus. Blood leaves the glomerulus through the efferent arteriole, then forms the peritubular capillaries and vasa recta that wrap the tubules before draining into the renal vein and IVC.

The Nephron — The Functional Unit

Each kidney contains roughly one million nephrons. Every nephron begins with a glomerulus (a tuft of fenestrated capillaries surrounded by Bowman's capsule) that ultrafilters plasma under the driving force of afferent arteriolar pressure. The filtrate then traverses the proximal convoluted tubule (PCT), where roughly 65% of filtered Na⁺, water, glucose, amino acids, phosphate, and bicarbonate are reabsorbed; the thin descending and thick ascending limbs of the loop of Henle, which generate the medullary concentration gradient via countercurrent multiplication and reabsorb another 25% of Na⁺ through the NKCC2 transporter (the target of loop diuretics); the distal convoluted tubule (DCT), where the NCC cotransporter (target of thiazides) fine-tunes Na⁺ reabsorption and calcium handling is regulated; and finally the collecting duct, where principal cells respond to aldosterone (ENaC channel — target of amiloride/spironolactone) and antidiuretic hormone (ADH/vasopressin opens aquaporin-2 channels), and intercalated cells handle final acid-base trimming.

Glomerular Filtration & RAAS

The glomerular filtration rate (GFR) is the volume of plasma filtered per minute (normal ~ 100–120 mL/min/1.73 m²) and is the single most important number in nephrology. It depends on renal plasma flow, the hydrostatic pressure across the glomerular capillary wall, and the integrity of the filtration barrier (endothelium → basement membrane → podocyte slit diaphragms). The juxtaglomerular apparatus — where the macula densa of the thick ascending limb contacts the afferent arteriole — senses distal Na⁺/Cl⁻ delivery and releases renin when perfusion falls. Renin cleaves angiotensinogen to angiotensin I; ACE converts it to angiotensin II, which constricts the efferent arteriole (preserving GFR when flow is low), stimulates aldosterone, promotes thirst and ADH release, and drives Na⁺ reabsorption in the PCT. This axis is why ACE inhibitors, ARBs, and mineralocorticoid antagonists sit at the center of nephrology therapeutics.

Endocrine Functions of the Kidney

Beyond filtration, the kidney is a major endocrine organ. The juxtaglomerular cells produce renin in response to low perfusion, sympathetic tone, or low distal Na delivery. The peritubular interstitial fibroblasts of the cortex produce erythropoietin (EPO) in response to hypoxia; loss of EPO production is the primary driver of anemia of CKD. The proximal tubule hydroxylates 25-hydroxyvitamin D to the active form 1,25-dihydroxyvitamin D (calcitriol) via 1-alpha-hydroxylase — a step progressively lost in CKD, producing the hypocalcemia, secondary hyperparathyroidism, and renal osteodystrophy that define CKD-MBD. The kidney also handles phosphate excretion under the control of FGF-23, which rises early in CKD and is increasingly recognized as a cardiovascular risk marker.

How GFR Is Estimated

Serum creatinine alone is a poor surrogate because it is affected by muscle mass, diet, and tubular secretion. eGFR is calculated from creatinine using the CKD-EPI 2021 equation, which removed the race coefficient and is now the standard in the US. Cystatin C (less muscle-dependent) is used as a confirmatory test when creatinine-based eGFR is unreliable (amputees, malnourished, cirrhotic, body-builders). Measured GFR using iothalamate, inulin, or iohexol clearance is reserved for research or borderline transplant donor evaluation.

02 Scribe Documentation Framework

Nephrology notes live at the intersection of internal medicine, critical care, and outpatient chronic disease management. A consult note on a hospitalized AKI patient, an outpatient CKD follow-up, a dialysis progress note, and a transplant clinic visit all have different rhythms but share one feature: every note is built around numbers. Creatinine trend, eGFR, potassium, bicarbonate, urine output, weight, and blood pressure show up in every assessment. Capture them exactly.

03 Acute Kidney Injury (AKI) Acute

Acute kidney injury is the abrupt decline in kidney function over hours to days. It is the bread-and-butter inpatient nephrology consult and is defined by the KDIGO 2012 AKI guidelines using serum creatinine and urine output criteria. AKI is classified mechanistically into three buckets: prerenal (reduced perfusion), intrinsic (parenchymal damage to glomeruli, tubules, interstitium, or vessels), and postrenal (obstruction).

KDIGO Definition & Staging

AKI is present when any one of the following occurs: increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours, increase in serum creatinine to ≥ 1.5 times baseline within the prior 7 days, or urine volume < 0.5 mL/kg/hr for 6 hours.

Historical Criteria: RIFLE & AKIN

Before KDIGO unified the field, two older systems were used; you will still see them in older notes and ICU charts.

Prerenal AKI

Prerenal AKI is a functional, reversible decline from reduced renal perfusion. The kidneys are structurally intact and simply under-pumped. Causes include true hypovolemia (GI losses, hemorrhage, diuretics, burns), effective hypovolemia (heart failure, cirrhosis, nephrotic syndrome), hypotension/sepsis, renal artery stenosis, and medications that impair autoregulation (NSAIDs constrict the afferent, ACEi/ARBs dilate the efferent). The laboratory signature is avid sodium reabsorption: FENa < 1%, urine Na < 20 mEq/L, urine osmolality > 500, and a BUN:Cr ratio > 20:1. Treatment is restoration of perfusion — crystalloid in true volume depletion, diuretics in congestive heart failure, albumin in cirrhosis, and holding offending drugs.

Postrenal AKI

Obstruction anywhere from the renal pelvis to the urethral meatus. In men, the most common cause is BPH; in women, pelvic malignancy. Bilateral obstruction (or unilateral with a single functioning kidney) is required to raise the creatinine. Bedside bladder scan and renal ultrasound looking for hydronephrosis are the diagnostic mainstays. Treatment is relief of obstruction: Foley catheter for bladder outlet obstruction, percutaneous nephrostomy or ureteral stent for upper tract obstruction. Watch for post-obstructive diuresis after relief.

Intrinsic AKI

Parenchymal damage. Subdivided by the injured compartment: tubular (ATN), interstitial (AIN), glomerular (glomerulonephritis), or vascular (atheroemboli, TMA, scleroderma renal crisis). Urinalysis with microscopy is the single most useful test — muddy brown granular casts suggest ATN, WBC casts with eosinophiluria suggest AIN, RBC casts with dysmorphic RBCs suggest glomerulonephritis.

04 ATN, AIN & Contrast Nephropathy Acute

Acute Tubular Necrosis (ATN)

ATN is the most common cause of inpatient intrinsic AKI. Prolonged ischemia (essentially prerenal that was not reversed) or nephrotoxins (aminoglycosides, vancomycin, amphotericin, cisplatin, heme pigment from rhabdomyolysis, myeloma light chains) damage the tubular epithelium, which sloughs into the lumen and forms the pathognomonic muddy brown granular casts. Laboratory signature: FENa > 2%, urine Na > 40, urine osmolality ~ 300 (isosthenuric because tubules cannot concentrate), BUN:Cr < 15. ATN follows a classic three-phase course: initiation (insult), maintenance (oliguric, days to weeks), and recovery (often polyuric — watch for hypokalemia and hypomagnesemia during this phase). Management is supportive: remove the offending insult, avoid further nephrotoxins, dose-adjust all medications, maintain euvolemia, and provide RRT if AEIOU criteria are met.

Acute Interstitial Nephritis (AIN)

AIN is a hypersensitivity inflammation of the renal interstitium, classically triggered by drugs: penicillins/cephalosporins, NSAIDs, PPIs, sulfonamides, rifampin, allopurinol, 5-ASA, and more recently immune checkpoint inhibitors. Infections (legionella, leptospira, CMV) and autoimmune disease (sarcoidosis, Sjögren) also cause AIN. The classic triad of fever, rash, and eosinophilia appears in < 10% of cases, so absence does not rule it out. Look for sterile pyuria, white-cell casts, subnephrotic proteinuria, and peripheral eosinophilia. Urine eosinophils are no longer considered sensitive or specific. Kidney biopsy is the gold standard when the diagnosis is not obvious. Treatment is prompt withdrawal of the offending drug; corticosteroids are often given for severe or non-recovering cases.

Contrast-Associated AKI (CA-AKI)

Iodinated contrast can cause AKI via direct tubular toxicity and medullary vasoconstriction, typically presenting as a creatinine rise within 24–48 hours of exposure that peaks at 3–5 days and resolves within 7–10 days. Recent evidence suggests the effect is smaller than historically feared; the current ACR/NKF consensus statement distinguishes contrast-associated AKI (temporal association) from contrast-induced AKI (causally proven) and supports isotonic crystalloid prophylaxis for high-risk patients (eGFR < 30). N-acetylcysteine is no longer recommended.

05 Rhabdomyolysis & Hepatorenal Syndrome Acute

Rhabdomyolysis

Skeletal muscle breakdown releases myoglobin, which precipitates in the tubules and causes a pigment nephropathy form of ATN. Triggers include crush injury, prolonged immobilization ("long lie"), seizures, extreme exertion, statins/fibrates, cocaine/stimulants, and inherited metabolic myopathies. Presentation is muscle pain, weakness, and tea-colored urine. Laboratory: massively elevated CK (often > 5,000 and frequently > 50,000), hyperkalemia, hyperphosphatemia, hypocalcemia (calcium deposits in damaged muscle), elevated uric acid, elevated LDH, elevated AST, and a UA that is "blood positive" on dipstick but shows no RBCs on microscopy (myoglobin cross-reacts). Treatment is aggressive isotonic fluid resuscitation (target urine output 200–300 mL/hr), correction of electrolytes, and monitoring for compartment syndrome.

Hepatorenal Syndrome (HRS)

HRS is AKI in the setting of advanced cirrhosis driven by splanchnic vasodilation, effective hypovolemia, and intense renal vasoconstriction. The kidneys are structurally normal. Diagnosis requires cirrhosis with ascites, AKI, no improvement after 48 hours of albumin and diuretic withdrawal, absence of shock, no recent nephrotoxins, and no structural kidney disease (bland urine, no or minimal proteinuria). HRS-AKI (formerly Type 1) is rapid and carries a dismal prognosis; HRS-NAKI (formerly Type 2) is slower. Treatment is albumin 1 g/kg/day plus a splanchnic vasoconstrictor: terlipressin (FDA-approved 2022), or norepinephrine (ICU), or midodrine + octreotide (floor). Definitive therapy is liver transplant.

06 Chronic Kidney Disease (CKD) Chronic

CKD is defined by KDIGO 2024 CKD guidelines as abnormalities of kidney structure or function present for > 3 months with implications for health. The diagnosis requires either GFR < 60 mL/min/1.73 m² OR markers of kidney damage (albuminuria UACR ≥ 30, urine sediment abnormalities, electrolyte abnormalities, histologic abnormalities, structural abnormalities by imaging, or kidney transplant). CKD is staged by both GFR (G1–G5) and albuminuria (A1–A3) — the so-called "heat map" — because albuminuria is an independent driver of progression and cardiovascular risk. USPSTF screening guidance and KDIGO recommend screening high-risk patients (diabetes, hypertension, cardiovascular disease, family history) with eGFR and UACR.

CKD Complications — The "CKD Bundle"

Every CKD progress note addresses the same cluster of problems:

• Hypertension: Target < 120/80 by 2021 KDIGO BP in CKD guideline when tolerated. ACEi or ARB is first line if albuminuria is present.
• Proteinuria: RAAS blockade + SGLT2 inhibitor (dapagliflozin or empagliflozin) independent of diabetes, per the DAPA-CKD and EMPA-KIDNEY trials.
• Anemia of CKD: Decreased EPO production; target Hgb 10–11.5 with ESAs (epoetin alfa, darbepoetin) and iron repletion (IV ferric gluconate, sucrose, or carboxymaltose). Never exceed Hgb 11.5 (increased CV risk).
• CKD-Mineral and Bone Disorder (CKD-MBD): Phosphate retention → FGF-23 rise → calcitriol suppression → secondary hyperparathyroidism → renal osteodystrophy. Manage with dietary phosphate restriction, phosphate binders (sevelamer, lanthanum, calcium acetate, ferric citrate), active vitamin D analogs (calcitriol, paricalcitol), and calcimimetics (cinacalcet, etelcalcetide) when PTH remains high.
• Metabolic acidosis: Treat when HCO₃ < 22 with oral sodium bicarbonate.
• Hyperkalemia: Dietary restriction, loop diuretic, potassium binders (patiromer, sodium zirconium cyclosilicate) to enable RAAS blockade continuation.
• Dyslipidemia: Statin for most CKD patients > 50 years.
• Vaccinations: Hepatitis B (double dose), pneumococcal, influenza, COVID-19.

07 Diabetic & Hypertensive Kidney Disease Chronic

Diabetic Kidney Disease (DKD)

Diabetes is the leading cause of CKD and ESRD in the United States. DKD progresses through predictable stages: hyperfiltration → microalbuminuria (A2) → overt proteinuria (A3) → declining GFR → ESRD, typically over 10–20 years. Pathology shows mesangial expansion, glomerular basement membrane thickening, and in advanced cases nodular glomerulosclerosis (Kimmelstiel-Wilson nodules). Annual screening with UACR and eGFR is standard of care for all diabetic patients. Management is built on the four pillars: (1) glycemic control (A1C individualized 6.5–8%), (2) ADA SGLT2i recommendation for eGFR ≥ 20 regardless of A1C, (3) RAAS blockade (ACEi or ARB) titrated to maximum tolerated dose, and (4) non-steroidal MRA finerenone (Kerendia) for residual albuminuria, based on the FIDELIO-DKD and FIGARO-DKD trials. GLP-1 agonists (semaglutide, tirzepatide) provide additional cardiorenal benefit.

Hypertensive Nephrosclerosis

Long-standing hypertension produces arteriolar hyalinosis and ischemic glomerulosclerosis. It is the second leading cause of ESRD and disproportionately affects Black Americans (associated with APOL1 risk variants). Presentation is slowly progressive CKD with mild proteinuria (usually < 1 g/day), bland urinary sediment, and small echogenic kidneys on ultrasound. Management is aggressive BP control (target < 120/80 per KDIGO) with ACEi/ARB and additional agents as needed. Biopsy is rarely performed unless atypical features are present.

08 Nephrotic Syndrome Glomerular

Nephrotic syndrome is the clinical pentad of heavy proteinuria (> 3.5 g/day), hypoalbuminemia (< 3.0 g/dL), edema, hyperlipidemia, and hypercoagulability (loss of antithrombin III, protein C/S). Patients present with frothy urine, peripheral and periorbital edema, and sometimes acute DVT, renal vein thrombosis, or PE. Kidney biopsy is usually required for definitive diagnosis in adults. The KDIGO 2021 glomerular disease guidelines standardize management.

Secondary Causes

Nephrotic syndrome is frequently a manifestation of a systemic disease. Diabetes is by far the most common cause in adults and usually does not require biopsy when the clinical picture fits. Amyloidosis (AL from plasma cell dyscrasia, AA from chronic inflammation) presents with nephrotic-range proteinuria, apple-green birefringence on Congo red staining, and often cardiac, GI, or neurologic involvement. Other secondary causes include HIV (collapsing FSGS), hepatitis B (membranous), hepatitis C (cryoglobulinemic MPGN), SLE (any class), solid and hematologic malignancies, and drugs (NSAIDs, pamidronate, heroin, interferon).

Management Principles

Every nephrotic patient receives RAAS blockade for proteinuria reduction, loop diuretics (often high-dose, sometimes IV) for edema, statin for hyperlipidemia, dietary sodium restriction, and prophylactic anticoagulation when albumin is profoundly low (< 2.0–2.5) or membranous nephropathy is present. Disease-specific immunosuppression depends on the biopsy diagnosis and risk stratification. Document response by serial UPCR/UACR, serum albumin, weight, and eGFR.

09 Nephritic Syndrome & Glomerulonephritis Glomerular

Nephritic syndrome is the classic "active urine" presentation: hematuria with dysmorphic RBCs and RBC casts, subnephrotic proteinuria (usually < 3.5 g/day), hypertension, edema, and rising creatinine. Rapidly progressive glomerulonephritis (RPGN) is nephritic syndrome with doubling of creatinine over days to weeks and crescents on biopsy — a medical emergency requiring urgent biopsy and immunosuppression.

10 Polycystic Kidney Disease & Inherited Tubulopathies Genetic

Autosomal Dominant PKD (ADPKD)

ADPKD is the most common inherited kidney disease, caused by mutations in PKD1 (~85%, chromosome 16, earlier and more severe) or PKD2 (~15%, chromosome 4, milder). Progressive cyst formation leads to massive kidney enlargement, hypertension by the second to third decade, flank pain, hematuria, stones, UTIs, and ESRD by the fifth to seventh decade. Extra-renal manifestations include hepatic cysts, intracranial berry aneurysms (screen if family history), mitral valve prolapse, and colonic diverticula. Diagnosis is by ultrasound (age-adjusted Ravine criteria) or by genetic testing. Tolvaptan (a vasopressin V2 antagonist) slows progression in rapidly progressive ADPKD but requires liver function monitoring. Autosomal recessive PKD (ARPKD) is a childhood disease with congenital hepatic fibrosis.

Tuberous Sclerosis & Von Hippel-Lindau

Tuberous sclerosis complex produces renal angiomyolipomas (AMLs) that can bleed catastrophically above 4 cm — managed with mTOR inhibitors (everolimus) or embolization. Von Hippel-Lindau disease carries a lifetime risk of clear-cell renal cell carcinoma and requires surveillance imaging.

Other Hereditary Diseases

Alport syndrome (type IV collagen mutation) causes hereditary nephritis, sensorineural hearing loss, and anterior lenticonus. Fabry disease (X-linked alpha-galactosidase deficiency) causes proteinuric CKD, angiokeratomas, and neuropathic pain. Gitelman (DCT, NCC loss — mimics thiazide) and Bartter (TAL, NKCC2 loss — mimics loop diuretic) syndromes present with hypokalemic metabolic alkalosis.

11 Renal Tubular Acidosis (RTA) Tubular

RTA is a non-anion-gap metabolic acidosis caused by impaired renal acidification. Three classic types plus a fourth, each with a distinct mechanism and signature.

(Type 3 was a mixed distal/proximal form in infants and is no longer used clinically.) Treatment is oral bicarbonate/citrate replacement for Types 1 and 2 (with potassium replacement in Type 1), and fludrocortisone or loop diuretics plus dietary K restriction for Type 4.

12 Sodium & Water Disorders Electrolyte

Hyponatremia (Na < 135)

Hyponatremia is the most common electrolyte disorder in hospitalized patients and is almost always a problem of too much water, not too little sodium. Workup is stepwise: (1) check serum osmolality to confirm hypotonicity (and exclude pseudohyponatremia from hyperlipidemia/hyperproteinemia or translocational hyponatremia from hyperglycemia — correction: add 1.6–2.4 to Na for every 100 mg/dL glucose > 100); (2) assess volume status; (3) check urine osmolality and urine sodium.

Hypernatremia (Na > 145)

Hypernatremia is a water deficit. Causes include inadequate intake (bedbound elderly, altered mental status), insensible losses (fever, burns), GI losses (osmotic diarrhea), and diabetes insipidus (central vs nephrogenic — distinguished by response to DDAVP). Central DI responds to lithium discontinuation, trauma, or surgery; nephrogenic DI is caused by lithium, hypercalcemia, hypokalemia, or genetic V2 receptor defects. Treat with free water replacement (oral or D5W), correcting ≤ 10–12 mEq/L per 24 hours to avoid cerebral edema. Calculate the free water deficit: TBW × ((Na/140) − 1).

13 Potassium, Calcium, Magnesium & Phosphate Electrolyte

Hyperkalemia (K > 5.0)

Causes: pseudohyperkalemia (hemolyzed sample, fist clenching), transcellular shifts (acidosis, insulin deficiency, beta-blockers, succinylcholine, tumor lysis, rhabdomyolysis), decreased renal excretion (AKI, CKD, ACEi/ARB, MRA, NSAIDs, trimethoprim, heparin, calcineurin inhibitors, type 4 RTA), and increased intake. EKG progression: peaked T waves → PR prolongation → loss of P wave → widened QRS → sine wave → VF/asystole. Treatment sequence: (1) Stabilize the membrane with IV calcium gluconate or calcium chloride; (2) Shift K into cells with insulin + D50, beta-2 agonist (albuterol), and IV sodium bicarbonate if acidotic; (3) Remove K from the body with loop diuretics, potassium binders (patiromer, sodium zirconium cyclosilicate, SPS), and emergent hemodialysis if refractory or in ESRD.

Hypokalemia (K < 3.5)

Causes: GI losses (diarrhea, laxative abuse), renal losses (loop and thiazide diuretics, hyperaldosteronism, Bartter/Gitelman, RTA 1 and 2, hypomagnesemia), transcellular shift (insulin, beta-2 agonists, alkalosis, refeeding). EKG: U waves, flattened T waves, ST depression, arrhythmias. Replace IV at ≤ 10–20 mEq/hr peripherally (higher via central line with monitoring). Always replace magnesium simultaneously — you cannot fix hypokalemia in the setting of hypomagnesemia.

Calcium Disorders

Hypercalcemia: The two dominant causes are primary hyperparathyroidism (outpatient, mild, chronic) and malignancy (inpatient, severe, acute — PTHrP in squamous cell carcinoma, bone metastases, multiple myeloma, activated vitamin D in lymphoma). Other causes: granulomatous disease (sarcoid, TB), thiazides, vitamin D toxicity, milk-alkali syndrome, lithium, hyperthyroidism, immobilization. Symptoms: "stones, bones, groans, and psychiatric overtones" — nephrolithiasis, osteopenia, abdominal pain and constipation, altered mental status. Treatment: aggressive IV saline, loop diuretic once euvolemic, IV bisphosphonate (zoledronic acid) or denosumab, calcitonin (fast but tachyphylaxis), and hemodialysis for refractory cases. Always correct for albumin (add 0.8 for every 1 g/dL below 4.0) or measure ionized calcium.

Hypocalcemia: Causes include hypoparathyroidism (post-thyroidectomy, autoimmune), vitamin D deficiency, CKD, pancreatitis, hungry bone syndrome, hyperphosphatemia (tumor lysis, rhabdo), and sepsis. Symptoms: perioral numbness, tetany, Chvostek sign, Trousseau sign, QT prolongation, seizures. Treatment: oral or IV calcium (calcium gluconate IV) plus vitamin D.

Magnesium & Phosphate

Hypomagnesemia: Caused by GI and renal losses (PPIs are a major under-recognized cause, along with loop and thiazide diuretics, aminoglycosides, cisplatin, amphotericin, alcoholism). Produces refractory hypokalemia and hypocalcemia. Replace with IV MgSO₄.

Hypophosphatemia: Refeeding syndrome, DKA recovery, alcoholism, Fanconi syndrome. Severe (< 1.0) can cause respiratory muscle weakness and rhabdomyolysis. Replace with oral or IV potassium/sodium phosphate.

Hyperphosphatemia: CKD/ESRD, tumor lysis, rhabdo. Treated with dietary restriction and phosphate binders.

14 Acid-Base Disorders Electrolyte

Every nephrology consult includes an acid-base assessment. Use a stepwise approach:

High Anion Gap Metabolic Acidosis (HAGMA)

Classic mnemonic GOLD MARK: Glycols (ethylene, propylene), Oxoproline (chronic acetaminophen), L-lactate, D-lactate, Methanol, Aspirin, Renal failure (uremia), Ketoacidosis (DKA, AKA, starvation).

Non-Gap (Hyperchloremic) Metabolic Acidosis

Mnemonic HARDUPS: Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Ureteroenteric fistula, Pancreatic fistula, Saline (large-volume NS resuscitation). The urine anion gap (UNa + UK − UCl) helps distinguish: negative → GI losses (NH₄⁺ excretion intact); positive → RTA (impaired NH₄⁺ excretion).

Metabolic Alkalosis

Divided by chloride-responsiveness. Chloride-responsive (UCl < 20): vomiting, NG suction, diuretics (after the acute effect), post-hypercapnia, cystic fibrosis. Treated with volume and chloride repletion (normal saline, KCl). Chloride-resistant (UCl > 20): primary hyperaldosteronism, Cushing syndrome, Liddle syndrome, Bartter, Gitelman, severe hypokalemia, and exogenous mineralocorticoid excess (licorice). Treated by addressing the underlying driver.

Respiratory Disorders — Mentioned for Completeness

Respiratory acidosis results from hypoventilation (COPD exacerbation, neuromuscular disease, opioid overdose, OSA/obesity hypoventilation). Respiratory alkalosis results from hyperventilation (anxiety, pain, fever, sepsis, pulmonary embolism, salicylate toxicity — which classically produces a mixed respiratory alkalosis and anion-gap metabolic acidosis, a high-yield pattern). Always confirm acute vs chronic using the compensation formulas above — the chronicity dictates whether you are seeing full compensation or a true mixed disorder.

15 Nephrolithiasis (Kidney Stones) Urologic

Kidney stones affect ~10% of the US population. Presentation is sudden-onset unilateral flank pain radiating to the groin ("renal colic"), often with hematuria, nausea, and vomiting. Non-contrast CT of the abdomen/pelvis is the gold standard imaging; ultrasound is used in pregnancy.

Management of acute colic: IV fluids, NSAIDs (ketorolac, if renal function allows) ± opioids, antiemetics, and alpha-blocker (tamsulosin) for distal ureteral stones ≤ 10 mm. Stones < 5 mm usually pass spontaneously; 5–10 mm have variable passage rates; > 10 mm almost always require intervention (ureteroscopy with laser lithotripsy, ESWL, or PCNL for staghorns). Red flags requiring urgent urology: obstruction with infection (emergent decompression), AKI, solitary kidney, or intractable symptoms.

16 UTI, Pyelonephritis & Renal Artery Stenosis Mixed

UTI & Pyelonephritis

Cystitis presents with dysuria, frequency, urgency, and suprapubic discomfort without fever. Pyelonephritis adds fever, chills, flank pain, costovertebral angle tenderness, and often nausea/vomiting. E. coli causes ~80% of community-acquired cases. Complicated UTI (men, pregnancy, CKD, stones, catheters, immunosuppression, transplant) requires broader coverage and longer duration. Workup: UA with culture, CBC, BMP, and CT in complicated cases to assess for abscess, emphysematous pyelonephritis, or obstruction. Outpatient pyelonephritis is treated with fluoroquinolone or TMP-SMX (local resistance permitting) for 7–14 days; inpatient cases receive IV ceftriaxone, piperacillin-tazobactam, or a carbapenem.

Emphysematous & Complicated Pyelonephritis

Emphysematous pyelonephritis is a necrotizing infection with gas within the renal parenchyma, seen almost exclusively in poorly controlled diabetics and urinary obstruction; gas on CT is pathognomonic. Management is emergency broad-spectrum antibiotics, relief of obstruction, and often percutaneous drainage or nephrectomy. Renal and perinephric abscess requires drainage plus prolonged antibiotics. Xanthogranulomatous pyelonephritis is a chronic destructive form associated with obstruction and Proteus infection — surgical nephrectomy is usually required.

Renal Artery Stenosis (RAS)

RAS is unilateral or bilateral narrowing of the renal artery, most commonly from atherosclerosis (older patients, CV disease) or fibromuscular dysplasia (young women, "string-of-beads" appearance). Presentation: resistant hypertension, recurrent flash pulmonary edema (bilateral RAS), sudden increase in creatinine after starting ACEi/ARB, unilateral small kidney, abdominal bruit. Diagnosis: duplex ultrasound (peak systolic velocity > 200 cm/s), CTA, or MRA. The CORAL trial showed no benefit of stenting over medical therapy for atherosclerotic RAS in most patients; intervention is reserved for refractory cases, flash pulmonary edema, or FMD (which responds well to angioplasty).

17 Dialysis — HD, PD & Access Dialysis

Hemodialysis (HD)

Standard in-center HD runs 3× per week for 3–4 hours per session. Blood is pumped from the patient through a dialyzer (semi-permeable membrane) where solute diffuses down its gradient into dialysate flowing counter-current, and excess water is removed by ultrafiltration (hydrostatic pressure gradient). Prescription elements documented in every HD note: dialyzer type and surface area, blood flow rate (Qb, typically 300–450 mL/min), dialysate flow rate (Qd, typically 500–800 mL/min), dialysate composition (Na, K, Ca, bicarbonate baths), treatment duration, ultrafiltration goal (target weight), heparin dose, and access used.

Adequacy is assessed by Kt/V (target ≥ 1.2 per session) and urea reduction ratio (URR ≥ 65%). Common intra-dialytic complications: hypotension (most common — excessive UF, cardiac dysfunction), cramps, nausea, dialysis disequilibrium syndrome (rapid urea shifts in new patients), first-use reactions, air embolism, and arrhythmia. Home HD and nocturnal HD are increasingly offered options.

Peritoneal Dialysis (PD)

PD uses the patient's peritoneal membrane as the dialysis barrier. Dialysate is instilled through a Tenckhoff catheter, dwells for hours, then drains. Two modalities: CAPD (continuous ambulatory, 4–5 manual exchanges per day) and APD (automated, cycler overnight). Advantages: home-based, continuous, preserves residual kidney function, hemodynamically gentle. Disadvantages: peritonitis (the big one — classic presentation is cloudy effluent with WBC > 100 and > 50% neutrophils), exit-site/tunnel infection, mechanical catheter problems, loss of ultrafiltration over time, and encapsulating peritoneal sclerosis (rare, devastating).

Vascular Access

The KDOQI access hierarchy prioritizes AV fistula (native vein-to-artery, preferred, best patency and lowest infection) > AV graft (PTFE or biologic conduit when veins inadequate) > tunneled dialysis catheter (last resort due to infection and central stenosis risk). Common fistula configurations: radiocephalic (Brescia-Cimino, wrist), brachiocephalic, and brachiobasilic transposition. Document: side, configuration, maturity, thrill/bruit, signs of stenosis (pulsatile, high venous pressures), steal syndrome (distal ischemia), aneurysm, infection, and last intervention (angioplasty, thrombectomy).

18 Kidney Transplant Management Transplant

Kidney transplant is the definitive treatment for ESRD, offering superior survival and quality of life compared with dialysis. Sources: deceased donor (standard criteria, expanded criteria, donation after cardiac death) and living donor (related or unrelated). The graft is typically placed extraperitoneally in the iliac fossa with anastomosis to the external iliac vessels and the ureter to the bladder. The native kidneys are almost always left in place.

Induction & Maintenance Immunosuppression

Induction: basiliximab (IL-2R antagonist) for low-risk or rabbit antithymocyte globulin (rATG) for high-risk recipients. Maintenance "triple therapy": calcineurin inhibitor (tacrolimus >> cyclosporine) + antimetabolite (mycophenolate mofetil or mycophenolic acid) + corticosteroid (prednisone, often tapered or withdrawn). mTOR inhibitors (sirolimus, everolimus) are alternatives in patients with CNI toxicity or certain malignancies. KDIGO transplant guidelines guide management.

Rejection

Hyperacute (minutes, preformed antibodies, now rare due to crossmatching), acute cellular (days to months, T-cell mediated, treated with steroid pulse ± rATG), acute antibody-mediated (donor-specific antibody, C4d deposition on biopsy, treated with plasmapheresis, IVIG, rituximab), and chronic (months to years, interstitial fibrosis/tubular atrophy, transplant glomerulopathy). Any rise in creatinine triggers workup: tacrolimus level, BK virus PCR, CMV PCR, urine studies, renal ultrasound with Dopplers, and often allograft biopsy.

Early Postoperative Course

Immediate graft function is defined by a brisk urine output and rapid creatinine fall. Delayed graft function (DGF) — requirement for dialysis within the first week — is more common with deceased-donor and expanded-criteria grafts and usually represents ischemia-reperfusion injury (ATN of the graft). Slow graft function is a partial form. Surgical complications to document include lymphocele, urine leak or ureteral stenosis, renal artery/vein thrombosis (emergency), and wound issues.

Transplant Complications & Monitoring

Infectious: CMV, BK polyomavirus (BK viremia → BK nephropathy), EBV/PTLD, pneumocystis (PJP prophylaxis with TMP-SMX), fungal, community infections. Malignancy: increased risk of skin cancer, PTLD, Kaposi, cervical. Cardiovascular disease remains the leading cause of death with a functioning graft. Recurrence of primary disease (FSGS, MPGN, IgA) is possible. Every transplant clinic note captures: days post-transplant, current immunosuppression (drug, dose, trough level), creatinine trend, BK/CMV status, infection/malignancy surveillance, BP, glycemic control (new-onset diabetes after transplant), and adherence.

19 Nephrology Procedures Procedural

Dialysis Prescription Elements

Every inpatient HD order specifies: treatment duration, target ultrafiltration (by dry weight), dialyzer type, Qb, Qd, dialysate K bath (1, 2, 3, or 4 mEq/L), dialysate Ca bath (2.5 or 3.0 mEq/L), dialysate Na (often 138–140), bicarbonate bath, heparin dose (loading and maintenance, or "tight heparin" / heparin-free), access, and any medications to give on dialysis (IV iron, ESA, vitamin D analog, antibiotics).

20 Labs, Urinalysis & Imaging Diagnostics

Urinalysis & Sediment

The urinalysis is the nephrologist's EKG. Dipstick captures pH, specific gravity, blood, protein, glucose, ketones, leukocyte esterase, nitrite, bilirubin, and urobilinogen. Microscopy captures RBCs (dysmorphic suggests glomerular origin), WBCs, epithelial cells, and the critical casts:

Proteinuria Quantification

24-hour urine collection is the historical gold standard but is prone to collection error. The spot urine protein-to-creatinine ratio (UPCR) and urine albumin-to-creatinine ratio (UACR) are more practical and correlate well with 24-hour values. UACR is preferred for CKD staging and monitoring. Nephrotic-range proteinuria is UPCR > 3.5 g/g or UACR > 2,200 mg/g.

FENa & FEUrea

FENa = (UNa × PCr) / (PNa × UCr) × 100. < 1% suggests prerenal or early glomerulonephritis; > 2% suggests ATN. FENa is unreliable in patients on diuretics — use FEUrea instead (< 35% is prerenal).

Serum Chemistries — The Basic Metabolic Panel

Every nephrology note is built on the BMP. Normal reference ranges vary slightly by lab, but the values a scribe must know cold are: Na 135–145, K 3.5–5.0, Cl 98–108, HCO₃ 22–28, BUN 8–20, Cr 0.6–1.2 (varies by sex and muscle mass), glucose 70–99 fasting, Ca 8.5–10.5, Mg 1.7–2.2, Phos 2.5–4.5, albumin 3.5–5.0. Critical values that trigger immediate action: K < 3.0 or > 6.0, Na < 120 or > 160, Ca < 7.0 or > 12.0, Mg < 1.0, Phos < 1.0, HCO₃ < 15.

Imaging

Renal ultrasound is the first-line imaging for AKI/CKD: assesses size (small < 9 cm suggests chronic disease), echogenicity (increased in CKD), hydronephrosis (obstruction), cysts, masses, and stones. CT without contrast is gold standard for stones. CT with contrast or CTA evaluates masses and vascular anatomy (use cautiously in CKD). MRA evaluates renal arteries; avoid gadolinium in eGFR < 30 (nephrogenic systemic fibrosis risk with older agents; newer group II agents are considered safer). Nuclear renal scan (MAG3, DTPA) assesses differential function, obstruction, and transplant perfusion.

21 Medications You Must Know Medications

22 Physical Exam — The Renal Exam

The nephrology exam is dominated by volume assessment. Every patient, every visit, every note.

23 Abbreviations Master List

Diagnoses & Syndromes

Labs, Imaging & Calculations

Treatment & Access

24 Sample HPI Templates

These templates show the rhythm of a well-written nephrology HPI. Use them as patterns when you sit down to chart.

25 References & Sources

Clinical Practice Guidelines

Landmark Clinical Trials

Diagram & Figure Sources