IM SUMMARY

< = 7 days

What is the duration criterion for Acute Kidney Injury (AKI)?

7 days to < 3 months

What is the duration criterion for Acute Kidney Disease (AKD)?

= 3 months

What is the duration criterion for Chronic Kidney Disease (CKD)?

N/A

What is the duration parameter for Normal Kidney Function (NKD)?

Increase in sCr by >= 50% within 7 days, OR increase in sCr >= 0.3 mg/dL (26.5 umol/L) within 48 hours, OR oliguria for >= 6 hours

What are the functional criteria for AKI?

AKI, OR eGFR < 60 mL/min/1.73 m2, OR decrease in eGFR >= 35%, OR increase in sCr > 50% over baseline

What are the functional criteria for AKD?

eGFR < 60 mL/min/1.73 m2

What is the functional criterion for CKD?

eGFR >= 60 mL/min/1.73 m2, stable sCr, and no oliguria

What are the functional criteria for Normal Kidney Function?

Not strictly required for diagnosis

What are the structural criteria for AKI?

Elevated markers of kidney damage such as albuminuria, hematuria, or pyuria

What are the structural criteria for AKD?

Elevated markers of kidney damage, with albuminuria being the most common

What are the structural criteria for CKD?

No markers of kidney damage

What are the structural criteria for Normal Kidney Function?

1.5 to 1.9 times baseline OR >= 0.3 mg/dL (>= 26.5 umol/L) increase

What is the sCr criterion for KDIGO AKI Stage 1?

< 0.5 mL/kg/h for 6 to 12 hours

What is the Urine Output criterion for KDIGO AKI Stage 1?

2.0 to 2.9 times baseline

What is the sCr criterion for KDIGO AKI Stage 2?

< 0.5 mL/kg/h for >= 12 hours

What is the Urine Output criterion for KDIGO AKI Stage 2?

3.0 times baseline OR increase in sCr to >= 4.0 mg/dL (>= 353.6 umol/L) OR initiation of KRT OR eGFR < 35 in patients < 18 years old

What is the sCr criterion for KDIGO AKI Stage 3?

< 0.3 mL/kg/h for >= 24 hours OR Anuria for >= 12 hours (< 100 mL/day)

What is the Urine Output criterion for KDIGO AKI Stage 3?

Renal hypoperfusion ("Supply problem") without parenchymal damage

What is the primary pathophysiology of Prerenal Azotemia?

Hypovolemia, decreased cardiac output (CHF, Cirrhosis), and impaired autoregulation (NSAIDs, ACEi/ARBs, Cyclosporine)

What are common clinical etiologies of Prerenal Azotemia?

Rapidly reversible upon restoration of hemodynamics, Urine Na < 20 mEq/L, and Urine SG > 1.018

What are key diagnostic clues for Prerenal Azotemia?

Direct structural damage to glomeruli, tubules, interstitium, or vessels

What is the primary pathophysiology of Intrinsic AKI?

Prolonged ischemic prerenal injury, sepsis, nephrotoxins, glomerulonephritis, vasculitis, and acute interstitial nephritis

What are common clinical etiologies of Intrinsic AKI?

Parenchymal tissue injury with urine sediment showing specific casts such as muddy brown or RBC casts

What are key diagnostic features of Intrinsic AKI?

Urinary tract outflow obstruction causing back-pressure into parenchyma

What is the primary pathophysiology of Postrenal AKI?

Bladder outlet obstruction (BPH, prostate cancer), bilateral pelviureteral obstruction, solitary kidney obstruction, and clogged catheter

What are common clinical etiologies of Postrenal AKI?

Bilateral obstruction or obstruction of a solitary functioning kidney

What anatomical state is required for postrenal obstruction to cause clinically significant elevated creatinine?

Low Perfusion

What is the physiological trigger for the Myogenic Reflex?

Vasodilation

What is the effect of the Myogenic Reflex on the afferent arteriole?

No effect

What is the effect of the Myogenic Reflex on the efferent arteriole?

Maintains GFR during acute perfusion drops

What is the net effect of the Myogenic Reflex on GFR?

Low NaCl

What is the physiological trigger for Tubuloglomerular Feedback?

Vasodilation

What is the effect of Tubuloglomerular Feedback on the afferent arteriole?

Vasoconstriction via Renin-Angiotensin II

What is the effect of Tubuloglomerular Feedback on the efferent arteriole?

Increases intraglomerular pressure and restores GFR

What is the net effect of Tubuloglomerular Feedback on intraglomerular pressure and GFR?

Inhibits renal prostaglandins leading to vasoconstriction

What is the effect of NSAIDs on the afferent arteriole?

No direct effect

What is the effect of NSAIDs on the efferent arteriole?

Decreases GFR and impairs the afferent vasodilation response

What is the net effect of NSAIDs on GFR?

No direct effect

What is the effect of ACE Inhibitors / ARBs on the afferent arteriole?

Blocks Angiotensin II leading to vasodilation

What is the effect of ACE Inhibitors / ARBs on the efferent arteriole?

Decreases GFR and reduces efferent arteriolar resistance

What is the net effect of ACE Inhibitors / ARBs on GFR?

Contrast-induced AKI

What clinical manifestation is caused by high-osmolar contrast media?

Nephrogenic Systemic Fibrosis (NSF) in advanced CKD

What condition is caused by Group 1 Gadolinium exposure?

Vancomycin, Amphotericin B, Aminoglycosides (Gentamicin, Amikacin), Acyclovir, Tenofovir, and Rifampin

Which antimicrobials act as nephrotoxic agents?

Direct tubular toxicity causing Acute Tubular Necrosis (ATN) or Acute Interstitial Nephritis (AIN)

What is the mechanism of antimicrobial nephrotoxicity?

Cisplatin, Carboplatin, Ifosfamide, Bevacizumab, and Immune Checkpoint Inhibitors

Which chemotherapeutic agents cause nephrotoxicity?

Tubular damage

What renal toxicity is caused by Cisplatin and Carboplatin?

Hemorrhagic cystitis

What specific complication is caused by Ifosfamide?

Vascular injury, hypertension, and proteinuria

What clinical manifestations are caused by Bevacizumab?

Ethylene glycol, Melamine, and Aristolochic acid

Which toxic ingestions cause nephrotoxicity?

Crystal-induced tubular obstruction and progressive tubulointerstitial nephritis

What is the mechanism of damage from toxic ingestions like ethylene glycol and aristolochic acid?

Myoglobin and Uric acid

Which endogenous substances act as renal toxins?

Myoglobinuria from rhabdomyolysis or hemolysis

What causes myoglobin-induced renal injury?

Uric acid crystallization in Tumor Lysis Syndrome

What causes uric acid-induced renal injury?

Pigmented, granular tubular epithelial cell debris

What is the microscopic appearance of Muddy Brown Casts?

Acute Tubular Necrosis (ATN) or Ischemia-associated AKI

What do Muddy Brown Casts signify?

Erythrocytes embedded in a Tamm-Horsfall protein matrix

What is the microscopic appearance of Red Blood Cell (RBC) Casts?

Glomerular Disease or Acute Nephritic Syndrome

What do Red Blood Cell (RBC) Casts signify?

Deformed RBCs with ring blebs ("Mickey Mouse" ears)

What is the microscopic appearance of Acanthocytes?

Confirms glomerular origin of hematuria

What do Acanthocytes signify on urine sediment analysis?

Leukocytes embedded in tubular casts

What is the microscopic appearance of White Blood Cell (WBC) Casts?

Acute Pyelonephritis, Tubulointerstitial Infection, or Acute Interstitial Nephritis (AIN)

What do White Blood Cell (WBC) Casts signify?

Envelope-shaped or 8-faced bipyramidal crystals

What is the microscopic appearance of Calcium Oxalate Crystals?

Ethylene glycol toxicity or nephrolithiasis

What do Calcium Oxalate Crystals signify?

20:1

What is the BUN to Plasma Creatinine ratio in Prerenal Azotemia?

10–15:1

What is the BUN to Plasma Creatinine ratio in Intrinsic AKI (Oliguric ATN)?

< 20 mEq/L

What is the Urine Sodium level in Prerenal Azotemia?

40 mEq/L

What is the Urine Sodium level in Intrinsic AKI?

1.018

What is the Urine Specific Gravity in Prerenal Azotemia?

Fixed / Isoosmolar (~1.010)

What is the Urine Specific Gravity in Intrinsic AKI?

Normal with hyaline casts

What is the urine sediment finding in Prerenal Azotemia?

Muddy brown granular casts and tubular epithelial cells

What is the urine sediment finding in Intrinsic AKI?

PSGN and Acute GN

What are prototypical diseases of Nephritic Syndrome?

HTN, Edema, Oliguria/Azotemia

What is the key clinical triad of Nephritic Syndrome?

Mild to Moderate (< 3.5 g/day)

What is the proteinuria severity in Nephritic Syndrome?

Heavy hematuria, dysmorphic RBCs, and RBC casts

What are the hematuria and sediment findings in Nephritic Syndrome?

MCD, FSGS, MGN, and Diabetic Kidney Disease

What are prototypical diseases of Nephrotic Syndrome?

Heavy proteinuria, Hypoalbuminemia, Hypercholesterolemia, and Edema

What are the key clinical features of Nephrotic Syndrome?

Heavy (>= 3.5 g/day)

What is the proteinuria severity threshold for Nephrotic Syndrome?

Minimal to absent hematuria

What are the sediment findings in Nephrotic Syndrome?

Thin Basement Membrane Disease, Alport Syndrome, and Anti-GBM Disease

What are prototypical diseases of Basement Membrane Syndromes?

Structural collagen IV defects, with ocular and hearing defects in Alport Syndrome

What features characterize Basement Membrane Syndromes?

Moderate proteinuria

What is the proteinuria severity in Basement Membrane Syndromes?

Persistent microscopic hematuria

What are the hematuria findings in Basement Membrane Syndromes?

Goodpasture Syndrome

What is the prototypical disease of Pulmonary-Renal Syndrome?

Anti-GBM attack on renal and alveolar capillaries

What is the underlying pathophysiology of Pulmonary-Renal Syndrome?

Moderate proteinuria

What is the proteinuria severity in Pulmonary-Renal Syndrome?

Hematuria plus Catastrophic Hemoptysis

What are the key urinary and systemic findings in Pulmonary-Renal Syndrome?

ANCA Vasculitis and Hypertensive Nephrosclerosis

What are prototypical diseases of Glomerular Vascular Syndromes?

Systemic vasculitis, endothelial injury, and ischemic necrosis

What features define Glomerular Vascular Syndromes?

Variable proteinuria

What is the proteinuria severity in Glomerular Vascular Syndromes?

Hematuria, ischemic lesions, and vascular thrombosis

What are the hematuria and vascular findings in Glomerular Vascular Syndromes?

Effacement of podocyte foot processes and loss of charge selectivity

What is the pathogenesis of Minimal Change Disease (MCD)?

Normal glomeruli ("Nil lesion")

What is the Light Microscopy finding in Minimal Change Disease?

Negative

What is the Immunofluorescence finding in Minimal Change Disease?

Diffuse foot process effacement ("melted kisses")

What is the Electron Microscopy finding in Minimal Change Disease?

Peak incidence in children < 12 years old, pure nephrotic syndrome, and excellent response to glucocorticoids

What are the key clinical features and treatment response of Minimal Change Disease?

Epithelial podocyte detachment driven by hyperfiltration or nephron underdosing

What is the pathogenesis of Focal Segmental Glomerulosclerosis (FSGS)?

Segmental sclerosis and hyalinosis in < 50% of glomeruli

What is the Light Microscopy finding in FSGS?

Negative or non-specific IgM/C3 in sclerotic areas

What is the Immunofluorescence finding in FSGS?