Clinical Mastery Series — 14 Deep-Dive Reviews
Updated March 2026 · Incorporates KDIGO 2026 AKI/AKD Guidelines
Andrew Bland, MD, FACP, FAAP
Medical Associates Dept of Nephrology · UICOMP · UDPA · Butler COM
Systematic AKI recognition, staging, and differential diagnosis
KDIGO 2026 staging, creatinine limitations, urinalysis interpretation (casts, FeNa confounders), renal ultrasound performance, Perazella-Coca score, and the CMS HH-AKI quality measure (mandatory 2027).
From clinical suspicion to kidney biopsy: urine sediment red flags, AIN vs GN differentiation, serologic workup, Perazella-Muriithi AIN score, biopsy interpretation, and diagnostic algorithms.
Every cause — each drug class with its characteristic latency, infections, systemic and autoimmune disease, malignancy, and the genetic tubulointerstitial diseases — then treatment sorted by etiology with an explicit “do NOT” column. Each claim tagged EVIDENCE-BASED or PRACTICE-BASED; 31 verified references.
Pre-renal, intrinsic, and post-renal mechanisms with evidence-based management
True hypovolemia vs EABV depletion, Ronco CRS classification (Types 1-5), hepatorenal syndrome pathophysiology, terlipressin evidence, the creatinine paradox of decongestion, and furosemide stress test.
S3 segment vulnerability, ischemia-reperfusion cascade, sublethal injury concept, three-leak oliguria model, ischemic vs nephrotoxic ATN, pigment nephropathy, and recovery phases.
Imaging modality selection (ultrasound, CT, MRU, Lasix renogram), diagnostic pitfalls, post-obstructive diuresis management, and evidence-based urology referral triggers.
Idiopathic vs secondary RPF, IgG4-RD pathophysiology, imaging characteristics, tissue biopsy, corticosteroid and rituximab therapy, ureteral stenting, and surveillance.
Genetic causes, muscle biopsy interpretation, genetic testing strategies, comprehensive gene-disorder mapping, clinical implementation, and pigment nephropathy management.
Mechanism-based framework for nephrotoxin identification and management
Mechanism classification (hemodynamic, ATN, AIN, crystal, TMA, osmotic), epidemiology, high-risk populations, polypharmacy syndrome, triple whammy, and systematic identification.
COX inhibition mechanisms, hemodynamic AKI, acute interstitial nephritis, the "triple whammy," dose-dependent CKD progression, Baker-Perazella risk-benefit framework, and CKD-stage prescribing guidance.
Class-by-class nephrotoxicity: aminoglycosides, vancomycin (AUC-guided dosing), beta-lactams, polymyxins, fluoroquinolones, sulfonamides, amphotericin B. Includes piperacillin-tazobactam/vancomycin synergy data.
COMPASS trial analysis, PPI-induced AIN pathophysiology, delayed presentation patterns, observational vs RCT evidence for CKD progression, urine biomarkers (IL-9, TNF-alpha), and deprescribing strategies.
Evidence-based KRT timing, modality selection, and supportive care
ELAIN, AKIKI, IDEAL, STARRT-AKI trial synthesis; early vs delayed initiation; CRRT vs IHD vs SLED modality selection; fluid overload thresholds; LIBERATE-D protocol.
Evidence against diuretics for ATN treatment, furosemide stress test protocol and diagnostic performance (sensitivity 81%, specificity 88%), RenalGuard nephroprotection, and RRT timing guidance.
This site teaches both staging systems. The lecture module uses the 2026 three-axis framework (function, urine output, biomarker); the Primer chapter and student handouts use 2012 single-axis staging. This bridge translates between them in both directions, with worked examples, and says plainly where each still governs — 2012 remains the exam answer and the logic behind institutional AKI e-alerts.
© 2026 Urine Nephrology Now — Andrew Bland, MD, FACP, FAAP
Clinical Mastery Series · AKI Advanced Module · Updated March 2026