The Nephron Under Attack
Different drugs injure different parts of the filtration unit. Walk the nephron from glomerulus to collecting duct and light up the agents that strike each segment — then localize injury with the biomarkers below.
Biomarkers that localize the injury
Creatinine rises late and lies often. These markers report on filtration, structure and segment-level function — telling you not just whether the kidney is hurt, but where.
Serum creatinine
Standard but insensitive — rises only after substantial GFR loss; confounded by muscle mass and cachexia.
eGFR
Used for CKD staging and chemotherapy dosing; unreliable in low-muscle, cachectic patients.
Cystatin C
Useful when creatinine misleads — sarcopenia, cachexia.
KIM-1
Rises early, before creatinine, in direct tubular damage.
NGAL
Detectable in urine and plasma hours before a creatinine bump.
Urine output
Part of the KDIGO/RIFLE criteria; oliguria flags AKI independently.
Electrolyte pattern
Magnesium wasting points distal; a full Fanconi picture points proximal.
Urine sediment
Granular casts (ATN), white cells (AIN), crystals (crystal nephropathy), schistocytes (TMA).
Tumor Lysis Syndrome
Massive tumor-cell breakdown — spontaneous or triggered by treatment — floods the blood with uric acid, phosphate and potassium. Uric acid and calcium-phosphate crystals then precipitate inside the tubular lumen, obstructing flow and triggering AKI, usually 48–72 hours after therapy begins. Highest risk: bulky, fast-dividing, chemo-sensitive tumors such as Burkitt lymphoma, ALL and AML.
Howard et al., NEJM 2011 · PMID 21561350- Uric acid. Precipitates in acidic tubular fluid → obstruction
- Phosphate. Calcium-phosphate crystals deposit in the lumen
- Potassium. Acute hyperkalemia — the lethal early threat