White Coat Companion: Renal Medicine and Urology

Comprehensive vocabulary flashcards reviewing renal medicine, nephrology, and urology concepts from White Coat Companion (2024-2025).

Total Body Water (TBW) Distribution

Estimated at $60\%$ of body weight, composed of $\frac{2}{3}$ intracellular fluid (ICF, $67\%$\text{ of TBW}) and $\frac{1}{3}$ extracellular fluid (ECF, $33\%$\text{ of TBW}). Plasma accounts for $25\%$ of ECF.

4/2/1 Rule

Formula for calculating hourly maintenance fluid infusion rates: $4\,\text{mL/kg/hr}$ for the first $10\,\text{kg}$, $2\,\text{mL/kg/hr}$ for the next $10\,\text{kg}$, and $1\,\text{mL/kg/hr}$ for each remaining kilogram.

100/50/20 Rule

Formula for calculating daily maintenance fluid volumes: $100\,\text{mL/kg/day}$ for the first $10\,\text{kg}$, $50\,\text{mL/kg/day}$ for the next $10\,\text{kg}$, and $20\,\text{mL/kg/day}$ for each remaining kilogram.

Pseudohyponatremia

An artifactual low serum sodium measurement resulting from elevated levels of serum lipids or proteins (e.g., hyperlipidemia, monoclonal gammopathy) despite normal measured serum osmolality ($275\text{--}295\,\text{mOsm/kg}$).

Osmotic Demyelination Syndrome

Irreversible central demyelination (often affecting the pons) caused by overly rapid correction of severe, chronic hyponatremia ($< 120\,\text{mEq/L}$); presents $2\text{--}5\,\text{days}$ later with dysphagia, dysarthria, paralysis, altered mental status, or locked-in syndrome.

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

Inappropriately elevated ADH secretion resulting in euvolemic hypotonic hyponatremia, high urine osmolality ($> 100\,\text{mOsm/kg}\,\text{H}_2\text{O}$), and elevated urine sodium ($\text{U}_{\text{Na}} > 40\,\text{mEq/L}$).

Peaked T Waves

Tall, symmetric, narrow electrocardiographic waves indicative of severe hyperkalemia ($\text{K}^+ > 5.0\,\text{mEq/L}$, commonly striking at $> 7.0\,\text{mEq/L}$), preceding PR/QRS widening and sinus arrest.

Chvostek Sign

Tapping over the facial nerve in front of the ear triggers involuntary twitching or contraction of ipsilateral facial muscles, indicating neuromuscular hyperexcitability from hypocalcemia.

Trousseau Sign

Induction of carpal spasm by inflating a blood pressure cuff above systolic pressure for $3\,\text{minutes}$, indicative of hypocalcemia-induced neuromuscular excitability.

Milk-Alkali Syndrome

A condition resulting from excessive ingestion of absorbable alkali and calcium (such as antacids) causing renal vasoconstriction and decreased GFR; diagnosed by the classic triad of hypercalcemia, metabolic alkalosis, and acute kidney injury.

Familial Hypocalciuric Hypercalcemia (FHH)

An autosomal dominant disorder characterized by an abnormal calcium-sensing receptor (CaSR), leading to high serum calcium, normal or mildly elevated PTH, and inappropriately low urinary calcium excretion.

Calcium-Phosphate Product

The mathematical product of serum calcium and serum phosphate ($\text{Ca} \times \text{P}_i$); values exceeding $70\,\text{mg}^2/\text{dL}^2$ substantially increase the risk for metastatic ectopic soft tissue calcification.

Winter's Formula

Formula predicting respiratory compensation in metabolic acidosis: $\text{pCO}_2 = 1.5 [\text{HCO}_3^-] + 8 \pm 2$.

Delta-Delta Ratio (\Delta/\Delta)

Ratio of change in anion gap to change in serum bicarbonate ($\frac{\Delta \text{AG}}{\Delta [\text{HCO}_3^-]}$); values $< 0.4$ indicate normal anion-gap acidosis, $1\text{--}2$ indicate pure elevated anion-gap acidosis, and $> 2$ indicate concurrent metabolic alkalosis.

Urine Anion Gap (UAG)

Calculated as $[\text{Na}^+] + [\text{K}^+] - [\text{Cl}^-]$; negative in gastrointestinal bicarbonate loss and normal renal ammonium excretion, but positive in distal renal tubular acidosis (Type 1 and Type 4 RTAs).

RIFLE Criteria

Classification schema for acute kidney injury: Risk ($1.5\text{-fold} \uparrow$ creatinine or GFR $\downarrow 25\%$), Injury ($2.0\text{-fold} \uparrow$ creatinine or GFR $\downarrow 50\%$), Failure ($3.0\text{-fold} \uparrow$ creatinine or GFR $\downarrow 75\%$), Loss (loss of function $> 4\,\text{weeks}$), and ESRD (complete loss $> 3\,\text{months}$ requiring dialysis).

Muddy Brown Granular Casts

Pathognomonic urinalysis finding representing sloughed, necrotic tubular epithelial cells that coalesce within the lumen in acute tubular necrosis (ATN).

Calciphylaxis (Calcific Uremic Arteriopathy)

Severe skin ischemia and vascular calcification of dermal and adipose arterioles occurring in longstanding ESRD (often tied to hyperphosphatemia); manifests as intensely painful violaceous plaques and non-healing necrotic ulcers.

Acute Interstitial Nephritis (AIN)

Immune-mediated inflammation of the renal interstitium, most commonly secondary to drugs (NSAIDs, penicillins, PPIs, loop diuretics), presenting $1\text{--}3\,\text{weeks}$ post-exposure with AKI, fever, rash, eosinophilia, and urine WBC casts.

Renal Papillary Necrosis

Ischemic infarction of the renal papillae associated with NSAID abuse, sickle cell disease, or pyelonephritis; manifests with gross hematuria, colicky flank pain, and sloughed tissue in the urine.

Type 1 Renal Tubular Acidosis (Distal RTA)

Inability of alpha-intercalated cells in the distal tubule to secrete hydrogen ions, leading to hypokalemia, urine $\text{pH} > 5.5$, positive urine anion gap, low bicarbonate ($< 10\,\text{mEq/L}$), and calcium phosphate nephrolithiasis.

Type 2 Renal Tubular Acidosis (Proximal RTA)

Defective proximal tubule bicarbonate reabsorption, leading to hypokalemia, variable urine pH ($< 5.5$ once serum bicarbonate drops), negative urine anion gap, and associated Fanconi syndrome or heavy metal exposure.

Type 4 Renal Tubular Acidosis (Hyperkalemic RTA)

Hypoaldosteronism or aldosterone resistance leading to impaired distal sodium reabsorption and hydrogen/potassium excretion, characterized by hyperkalemia, urine $\text{pH} < 5.5$, and positive urine anion gap.

Bartter Syndrome

Autosomal recessive dysfunction of the $\text{Na}^+-\text{K}^+-2\text{Cl}^-$ cotransporter in the thick ascending limb of Henle, mimicking chronic loop diuretic use with hypokalemia, metabolic alkalosis, and hypercalciuria.

Gitelman Syndrome

Autosomal recessive loss-of-function mutation in the $\text{Na}^+-\text{Cl}^-$ cotransporter of the distal convoluted tubule, mimicking thiazide diuretic use with hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria.

Liddle Syndrome

Autosomal dominant gain-of-function mutation in the epithelial sodium channel (ENaC) causing inappropriate sodium reabsorption; manifests as hypertension, hypokalemia, and metabolic alkalosis with suppressed aldosterone and renin.

Syndrome of Apparent Mineralocorticoid Excess (SAME)

Deficiency of $11\beta$-hydroxysteroid dehydrogenase type 2 (congenital or acquired from glycyrrhetinic acid in licorice), preventing conversion of cortisol to cortisone and causing cortisol-mediated mineralocorticoid receptor overactivation.

Fibromuscular Dysplasia (FMD)

Non-atherosclerotic angiopathy of medium-sized arteries commonly seen in young women, presenting with secondary hypertension, abdominal/carotid bruits, and a characteristic 'string of beads' appearance on angiography.

Dysmorphic Red Blood Cells

Erythrocytes with fragmented, distorted shapes or blebbing membranes (such as acanthocytes) seen on urine microscopy, establishing a glomerular origin of hematuria.

Post-Streptococcal Glomerulonephritis (PSGN)

Nephritic syndrome occurring $\sim 2\,\text{weeks}$ following group A beta-hemolytic Streptococcus skin or pharyngeal infection; characterized on light microscopy by enlarged hypercellular glomeruli and on electron microscopy by subepithelial 'humps' ($\text{IgG}$ and $\text{C3}$).

Rapidly Progressive Glomerulonephritis (RPGN)

Severe nephritic syndrome featuring rapid deterioration of renal function with crescent moon-shaped fibrin deposits filling Bowman space on histology; divided into Type I (anti-GBM), Type II (immune-complex), and Type III (pauci-immune/ANCA-associated).

Diffuse Proliferative Glomerulonephritis (DPGN)

Severe manifestation of lupus nephritis (Class IV) displaying extensive wire-looping of capillary loops on light microscopy and subendothelial immune complex deposition on electron microscopy.

Minimal Change Disease (MCD)

Most common cause of pediatric nephrotic syndrome, characterized by normal light microscopy, negative immunofluorescence, and diffuse podocyte foot process effacement on electron microscopy, responding dramatically to corticosteroids.

Focal Segmental Glomerulosclerosis (FSGS)

Most common cause of nephrotic syndrome in Black adults, characterized by segmental sclerosis and hyalinosis of glomeruli on light microscopy; can be primary or secondary to HIV ('collapsing variant'), sickle cell, or morbid obesity.

Membranous Nephropathy

Nephrotic disorder commonly caused by autoantibodies against the phospholipase A2 receptor (PLA2R) or secondary to hepatitis B/C, NSAIDs, or solid tumors; characterized by diffuse capillary wall thickening, 'spike and dome' subepithelial deposits, and granular immunofluorescence.

Alport Syndrome

X-linked defect in type IV collagen alpha chains resulting in 'basket-weave' longitudinal splitting of the glomerular basement membrane, progressive hematuria, sensorineural hearing loss, and ocular abnormalities.

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

Inherited mutation in PKD1 or PKD2 causing progressive expansion of bilateral renal cysts, hypertension, flank pain, hematuria, and extrarenal manifestations including berry aneurysms and hepatic cysts.

Calcium Oxalate Nephrolithiasis

The most common form ($80\%$) of kidney stone, forming radiodense envelope-shaped crystals in urine with $\text{pH} < 5.5$, often triggered by hypercalciuria, malabsorption, or ethylene glycol ingestion.

Struvite Calculi (Magnesium Ammonium Phosphate)

Radiodense 'coffin lid' stones forming in alkaline urine ($\text{pH} > 5.5$) secondary to urease-producing pathogens (e.g., Proteus, Klebsiella); commonly develop into massive staghorn calculi requiring percutaneous nephrolithotomy.

Stress Incontinence

Involuntary loss of urine resulting from pelvic floor weakness and urethral hypermobility, triggered by increased intra-abdominal pressure (e.g., coughing, sneezing, exercise) without nocturnal symptoms.

Urge Incontinence

Involuntary loss of urine preceded by a sudden, intense sensation to void caused by uninhibited detrusor muscle contractions, commonly accompanied by nocturnal wetting.

Interstitial Cystitis / Bladder Pain Syndrome

Chronic lower urinary tract and pelvic pain syndrome lasting $> 6\,\text{weeks}$ with dyspareunia, urinary frequency, and pain relief upon bladder emptying, occurring in the absence of documented bacterial infection.

Xanthogranulomatous Pyelonephritis

Severe chronic destructive granulomatous inflammation of renal parenchyma featuring abundant lipid-laden foamy macrophages, typically occurring in the setting of chronic obstruction by a staghorn calculus.

Von Hippel-Lindau (vHL) Disease

Autosomal dominant tumor suppressor gene deletion on chromosome 3p, predisposing to clear cell renal cell carcinomas, retinal and cerebellar hemangioblastomas, and pheochromocytomas.

Wilms Tumor (Nephroblastoma)

Most common pediatric renal malignancy, arising from embryonic nephrogenic blastema and linked to mutations in the WT1 gene on chromosome 11; presents as a large, smooth abdominal mass that rarely crosses the midline.

Vesicoureteral Reflux (VUR) Grading

System scoring retrograde urine flow on voiding cystourethrogram (VCUG) from Grade I (ureter only) to Grade V (massive ureteral dilatation, extreme caliceal tortuosity, and complete loss of renal papillary impressions).

Posterior Urethral Valves (PUV)

Obstructing congenital mucosal folds in the male posterior urethra, causing bilateral hydronephrosis, dilated thick-walled bladder, poor urinary stream, and high risk of chronic renal insufficiency.

Cryptorchidism

Failure of one or both testes to descend into the scrotum by $4\,\text{months}$ of age; managed by surgical orchiopexy before $1\,\text{year}$ of life to mitigate the long-term risk of infertility and testicular germ cell cancer.

Paraphimosis

Urologic emergency where a retracted prepuce becomes trapped behind the coronal sulcus, causing venous engorgement, severe pain, and progressive edema of the glans penis.

Testicular Torsion

Rotation of the spermatic cord and testis within the tunica vaginalis, causing sudden vascular occlusion, severe acute scrotal pain, high-riding transverse testis, and loss of the cremasteric reflex.

Prehn Sign

Physical maneuver where manual elevation of the painful testicle relieves pain in acute epididymitis, but does not relieve pain in testicular torsion.

Blue Dot Sign

A discrete, tender, blue-tinged nodule visible through the superior scrotal skin, pathognomonic for ischemic necrosis following torsion of the appendix testis.

Fournier Gangrene

Life-threatening polymicrobial necrotizing fasciitis of the perineum, scrotum, and perianal region; characterized by rapid progression of severe pain, tense edema, crepitus, and systemic septic shock.

Varicocele

Abnormal tortuous dilation of the pampiniform venous plexus, clinically described as a soft 'bag of worms' scrotal mass that decompresses in the recumbent position, predominating on the left side due to renal vein drainage.

Priapism

Persistent, involuntary, and painful penile erection lasting $\ge 4\,\text{hours}$ unrelated to sexual arousal; divided into low-flow (ischemic, treated with intracorporal phenylephrine) and high-flow (nonischemic/traumatic) etiologies.