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CKD Mineral Bone Disease

Hyperphosphatemia + hypocalcemia -> secondary hyperparathyroidism -> renal osteodystrophy (subperiosteal bone resorption).

Winter's Formula

Expected PaCO2 = 1.5 × [HCO3-] + 8 ± 2; if measured PaCO2 is higher -> concomitant respiratory acidosis; if lower -> respiratory alkalosis.

Nephrolithiasis Imaging

Non-contrast helical CT abdomen/pelvis is gold standard; renal ultrasound preferred in pregnancy to avoid radiation.

Uric Acid Stones

Radiolucent on plain radiograph; needle-shaped rhomboid crystals; acid urine pH < 5.5; alkalinize urine with potassium citrate.

Stepwise Acid-Base Interpretation Guide

DisorderPrimary AbnormalityCompensatory ResponseHigh-Yield Etiologies
High Anion Gap Metabolic Acidosis (HAGMA)Low HCO3- (< 24) with Anion Gap > 12 [Na - (Cl + HCO3)]Respiratory hyperventilation (Winter's: PaCO2 = 1.5 × HCO3 + 8 ± 2)GOLD MARK: Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin/salicylates, Renal failure (uremia), Ketoacidosis (DKA, starvation)
Normal Anion Gap (Hyperchloremic) AcidosisLow HCO3- with normal AG (≤ 12); high serum chlorideRespiratory hyperventilationHARDASS: Hyperalimentation, Acetazolamide, Renal tubular acidosis (RTA 1, 2, 4), Diarrhea (loss of bicarb), Spironolactone
Metabolic AlkalosisHigh HCO3- (> 28) with high arterial pH (> 7.45)Hypoventilation (PaCO2 rises ~0.7 mmHg per 1 mEq/L rise in HCO3-)Saline-responsive (Urine Cl < 20): Vomiting, nasogastric suction, loop/thiazide diuretics. Saline-resistant (Urine Cl > 20): Primary hyperaldosteronism, Cushing syndrome

Nephrolithiasis: Crystal Morphology & Management

Stone CompositionX-Ray & CT AppearanceMicroscopic Crystal Shape & Urine pHTreatment & Prevention Strategy
Calcium Oxalate (75–80%)Radiopaque on X-ray; white on CTEnvelope-shaped or dumb-bell; independent of pH; hypercalciuria / ethylene glycolHydration, thiazide diuretics (decrease urine calcium), low-sodium diet; do NOT restrict dietary calcium (calcium binds oxalate in gut)
Struvite (Ammonium Magnesium Phosphate)Radiopaque; forms massive staghorn calculi in renal pelvis'Coffin-lid' crystals; alkaline urine (pH > 7.0) due to urease-positive organisms (Proteus mirabilis, Klebsiella)Complete surgical eradication (percutaneous nephrolithotomy) + antimicrobial therapy; stone acts as foreign bacterial nidus
Uric Acid (5–10%)Radiolucent on X-ray; visible on non-contrast CTRhomboid or needle-shaped; acidic urine (pH < 5.5); gout, high cell turnover (tumor lysis)Urine alkalinization with potassium citrate; Allopurinol / Febuxostat for hyperuricemia
Cystine (1–2%)Faintly radiopaque on X-rayHexagonal crystals; positive sodium cyanide-nitroprusside test; autosomal recessive defect in COLA transporterHigh hydration (> 3–4 L/day), urine alkalinization (potassium citrate); chelating agents (tiopronin, penicillamine)
OMM Board Correlate: Renal Viscerosomatics & Ureteral Peristalsis
  • Renal Sympathetics: Originates from T10–T11 via least splanchnic nerve to aorticorenal ganglion. Acute ureteral stone passage causes severe unilateral paraspinal spasms at T10–L1.
  • Chapman Points for Kidneys: Anterior point is located 1 inch superior and 1 inch lateral to umbilicus. Posterior point between transverse processes of T12 and L1.
  • Psoas Spasm Correlation: The ureter courses directly across the anterior surface of the psoas major muscle; ureteral calculi induce reactive psoas hypertonicity (positive Thomas test on affected side).
Board Traps & Common Distractors
  • A kidney stone in the presence of systemic infection (fever, chills, leukocytosis, pyuria) constitutes an urological emergency (obstructive urosepsis); immediate emergent decompression via ureteral stent or percutaneous nephrostomy is required.
  • In patients with severe CKD, gadolinium contrast for MRI carries a substantial risk of Nephrogenic Systemic Fibrosis (NSF); avoid in GFR < 30 mL/min.
  • Stones < 5 mm typically pass spontaneously with medical expulsive therapy (Tamsulosin / alpha-blocker); stones > 10 mm require urological intervention (shock wave lithotripsy or ureteroscopy).