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Nephrology Exam Master Notes

1. ⭐⭐⭐⭐⭐ Chronic Kidney Disease (CKD)

Definition: Kidney damage or decreased kidney function persisting for ≥3 months, regardless of cause.

Primary marker: Glomerular Filtration Rate (GFR)
Other markers: proteinuria, abnormal urine/blood/imaging findings

Staging (KDIGO/NKF):

Stage	Description	GFR (mL/min/1.73 m²)
1	Kidney damage, normal GFR	≥90
2	Kidney damage, mild ↓ GFR	60-89
3	Moderate ↓ GFR	30-59
4	Severe ↓ GFR	15-29
5	Kidney failure (ESKD)	<15

GFR Calculation Formulas:

Cockcroft-Gault: CrCl = (140 - Age) × Weight / (72 × SCr) [× 0.85 if female]
MDRD: GFR = 1.86 × (SCr)^-1.154 × (Age)^-0.203 [× 0.742 if female; × 1.210 if Black]
CKD-EPI: More accurate at higher GFR values than MDRD

Causes:

Diabetic nephropathy (#1 cause globally)
Hypertension / hypertensive nephrosclerosis
Glomerulonephritis
Polycystic kidney disease
Recurrent UTIs / obstruction

Complications (AEIOU mnemonic):

Anemia (↓ EPO production)
Electrolyte abnormalities (hyperkalemia, metabolic acidosis, hyperphosphatemia)
Infection risk ↑
Osteodystrophy (renal bone disease - ↓ active Vit D, ↑ PTH, ↑ phosphate)
Uremia (nausea, pericarditis, encephalopathy, pruritis)

Management:

Treat underlying cause
ACE inhibitors / ARBs - reduce proteinuria and slow progression
Blood pressure control (<130/80 mmHg)
Low-protein diet, sodium restriction
Treat anemia with erythropoiesis-stimulating agents (ESAs) + iron
Phosphate binders, active Vitamin D (calcitriol)
Dialysis or transplantation at Stage 5

2. Acute Kidney Injury (AKI)

Definition (KDIGO criteria):

SCr rise ≥0.3 mg/dL within 48 hours, OR
SCr rise ≥1.5× baseline within 7 days, OR
Urine output <0.5 mL/kg/hr for >6 hours

Staging:

Stage	Creatinine	Urine Output
1	×1.5-1.9 baseline or ↑ ≥0.3 mg/dL	<0.5 mL/kg/hr for 6-12 h
2	×2.0-2.9 baseline	<0.5 mL/kg/hr for ≥12 h
3	×3 baseline or SCr ≥4.0 or KRT needed	<0.3 mL/kg/hr for ≥24 h or anuria ≥12 h

Classification (Pre-renal, Renal, Post-renal):

Type	Causes	BUN:Cr Ratio	FeNa
Pre-renal	Dehydration, heart failure, sepsis, hemorrhage	>20:1	<1%
Intrinsic renal	ATN (most common), glomerulonephritis, interstitial nephritis	10-20:1	>2%
Post-renal	Obstruction (BPH, calculi, tumor)	Variable	Variable

ATN (Acute Tubular Necrosis) - most common intrinsic cause:

Causes: ischemia (prolonged pre-renal) or nephrotoxins (aminoglycosides, contrast, myoglobin in rhabdomyolysis)
Classic finding: muddy brown granular casts in urine

Management:

Identify and treat underlying cause
IV fluids for pre-renal AKI
Avoid nephrotoxins
Manage complications: hyperkalemia, acidosis, fluid overload
Indication for emergency dialysis: AEIOU = Acidosis (severe), Electrolytes (hyperkalemia refractory), Ingestion (toxins), Overload (pulmonary edema), Uremia (symptoms)
Most AKI is reversible; ~25% hospitalized patients develop AKI; KRT needed in ~10%

AKI vs CKD: AKI = <3 months; CKD = ≥3 months. AKI increases long-term risk of CKD progression.

3. Nephrotic Syndrome

Definition (the classic tetrad):

Proteinuria >3.5 g/day (massive)
Hypoalbuminemia (<3 g/dL)
Edema (pitting, periorbital, dependent)
Hyperlipidemia + lipiduria (Maltese cross pattern on microscopy)

Pathophysiology: Loss of negative charge of glomerular basement membrane (GBM) → albumin leaks through → liver compensates with increased lipoprotein synthesis → hyperlipidemia + lipiduria

Primary Causes (memorize by age):

Cause	Key Feature	Population
Minimal Change Disease (MCD)	Normal LM, effacement of podocytes on EM	Children (#1), also adults with NSAIDs/lymphoma
Focal Segmental Glomerulosclerosis (FSGS)	Focal sclerosis, collapse	Adults, HIV, obesity, heroin
Membranous Nephropathy	Spike-and-dome on EM, subepithelial deposits	Adults #1, associated with Hep B, SLE, malignancy
Membranoproliferative GN (MPGN)	Tram-track appearance, subendothelial deposits	Associated with Hep C, complement disorders

Secondary Causes:

Diabetes (most common systemic cause)
SLE (Class V lupus nephritis)
Amyloidosis
Drugs: gold, penicillamine, NSAIDs, captopril, heroin

Complications:

Thromboembolism (loss of antithrombin III) - especially renal vein thrombosis
Infection (loss of immunoglobulins - encapsulated organisms)
Protein malnutrition
AKI

Treatment:

MCD: Corticosteroids (highly responsive - >90%)
Membranous: Steroids + cyclophosphamide or calcineurin inhibitors
FSGS: Steroids, cyclosporine
All: ACE/ARB (reduce proteinuria), statins, diuretics, anticoagulation if thrombotic risk high

4. Acute Glomerulonephritis (Nephritic Syndrome)

Definition - The classic pentad:

Hematuria (cola/tea-colored urine) - RBC casts on microscopy
Proteinuria (mild-moderate, <3.5 g/day)
Hypertension
Oliguria (decreased urine output)
Edema (periorbital > peripheral)

Key difference - Nephrotic vs Nephritic:

Feature	Nephrotic	Nephritic
Proteinuria	>3.5 g/day	<3.5 g/day
Hematuria	Absent	Present (RBC casts)
BP	Normal or ↑	↑↑
Edema	Massive	Mild
Hypoalbuminemia	Yes	No/mild
Mechanism	Podocyte damage	Inflammatory/proliferative

Causes:

Cause	Key Feature
Post-streptococcal GN (PSGN)	2-3 weeks after strep throat/skin infection; ↓C3, normal C4; lumpy-bumpy deposits on IF
IgA Nephropathy (Berger's)	#1 GN worldwide; hematuria 1-2 days after upper respiratory infection; mesangial IgA on IF
Goodpasture Syndrome	Anti-GBM antibodies; hemoptysis + nephritis; linear IgG on IF
ANCA-associated vasculitis	Wegener's (PR3-ANCA/c-ANCA), Microscopic polyangiitis (MPO-ANCA/p-ANCA); pauci-immune on IF
Lupus Nephritis	Full house pattern on IF; ↓C3 and ↓C4; anti-dsDNA

RBC casts = pathognomonic for glomerulonephritis (formed in renal tubules)

Treatment:

PSGN: Supportive (usually self-limiting)
Lupus: Steroids + mycophenolate or cyclophosphamide
Goodpasture/ANCA: Steroids + cyclophosphamide + plasmapheresis (for Goodpasture)

5. Diabetic Nephropathy

Most common cause of ESKD (End-Stage Kidney Disease) worldwide. Occurs in ~30-40% of patients with Type 2 diabetes.

Pathogenesis:

Hyperglycemia → advanced glycation end-products (AGEs) → GBM thickening
Hyperfiltration → glomerular hypertension → mesangial expansion
Activation of RAAS → TGF-β → fibrosis
Genetic susceptibility (ACE gene polymorphisms play a role)

Histological Stages (Kimmelstiel-Wilson lesion = pathognomonic):

Glomerular hypertrophy + hyperfiltration
GBM thickening + mesangial expansion
Nodular glomerulosclerosis (Kimmelstiel-Wilson nodules - PAS-positive eosinophilic nodules)
Advanced glomerulosclerosis, ESKD

Clinical Progression:

Stage	Feature
Early	Microalbuminuria (30-300 mg/day) = earliest marker
Intermediate	Macroalbuminuria (>300 mg/day), hypertension
Late	Declining GFR, nephrotic-range proteinuria
End-stage	ESKD requiring dialysis/transplant

Management:

Tight glycemic control (HbA1c <7%) - slows progression
ACE inhibitors / ARBs - first-line for proteinuria regardless of BP
SGLT2 inhibitors (empagliflozin, dapagliflozin) - reduce proteinuria + GFR decline
finerenone (non-steroidal MRA) - newer agent, reduces CKD progression
BP control <130/80 mmHg
Low-protein diet
Treat dyslipidemia (statins)
Retinopathy often coexists - check eyes

6. Hemodialysis (HD) & Peritoneal Dialysis (PD)

Hemodialysis (HD)

Principle: Blood passes through an extracorporeal circuit with a semipermeable membrane (dialyzer). Waste removed by diffusion (concentration gradient) and ultrafiltration (pressure gradient).

Access:

Arteriovenous fistula (AVF) - preferred (lowest infection risk, longest lasting)
AV graft - second choice
Tunneled central venous catheter - temporary/bridge

Schedule: Typically 3×/week, 3-4 hours per session

Adequacy: Measured by Kt/V (urea clearance); target ≥1.2 per session

Complications:

Hypotension (most common - due to rapid fluid removal)
Muscle cramps
Infection (especially with catheter)
Air embolism
Disequilibrium syndrome (cerebral edema from rapid urea removal - headache, seizures)
Long-term: amyloidosis (β2-microglobulin), cardiovascular disease

Peritoneal Dialysis (PD)

Principle: Peritoneum acts as the natural semipermeable membrane. Dialysate is infused into the peritoneal cavity; osmotic gradient (glucose) drives ultrafiltration.

Types:

CAPD (Continuous Ambulatory PD): 3-5 exchanges/day manually
APD (Automated PD): Machine performs exchanges overnight

Adequacy: Kt/V target ≥1.7/week

Complications:

Peritonitis - most serious/common; cloudy effluent, fever, abdominal pain; usually gram-positive organisms (Staph. epidermidis)
Catheter exit-site infection
Fluid overload / inadequate ultrafiltration
Hernias (↑ intraabdominal pressure)
Hyperglycemia (glucose in dialysate)
Protein loss

HD vs PD Comparison:

Feature	HD	PD
Membrane	Artificial	Peritoneum
Location	In-center (mainly)	Home
Frequency	3×/week	Daily
Vascular access	Required	Not needed
Anticoagulation	Heparin needed	Not needed
Main complication	Hypotension	Peritonitis
Residual kidney function	Lost faster	Better preserved
Survival	Similar	Similar
Preferred in	Cardiac failure, home unavailable	Home preference, vascular access issues, children, diabetics

PD is preferred over HD in: ADPKD (avoids heparin - reduces cyst bleeding risk), patients with poor vascular access, remote areas, children.

7. Renal Function Tests (RFTs)

Tests of Glomerular Function:

Test	Normal	Significance
Serum Creatinine	0.6-1.2 mg/dL (M); 0.5-1.1 mg/dL (F)	Rises when GFR drops >50% (insensitive early marker)
BUN (Blood Urea Nitrogen)	7-20 mg/dL	Affected by diet, hydration, liver function
BUN:Cr ratio	10-20:1	>20:1 = pre-renal; <10:1 = liver disease/malnutrition
eGFR	>60 mL/min/1.73m²	Best overall marker of kidney function
Creatinine Clearance (CrCl)	80-120 mL/min	Cockcroft-Gault equation
Cystatin C	0.5-1.0 mg/L	More sensitive than creatinine; unaffected by muscle mass

Tests of Tubular Function:

Urine specific gravity (1.001-1.035) - concentrating ability
Urine osmolality - concentrating/diluting ability
Fractional excretion of Na (FeNa) = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100

Urinalysis findings:

Finding	Significance
RBC casts	Glomerulonephritis
WBC casts	Pyelonephritis, interstitial nephritis
Granular casts	ATN ("muddy brown")
Waxy/broad casts	CKD (advanced)
Fatty casts / oval fat bodies	Nephrotic syndrome
Proteinuria	Glomerular/tubular damage

Proteinuria grades:

Microalbuminuria: 30-300 mg/day (earliest sign of glomerular damage, e.g., diabetic nephropathy)
Macroalbuminuria: >300 mg/day
Nephrotic range: >3.5 g/day

8. Electrolyte Disorders - Hyperkalemia

Definition: Serum K⁺ > 5.0-5.5 mEq/L

Causes (5 Rs):

Renal failure (most common) - impaired excretion
Redistribution - acidosis (H⁺ in, K⁺ out), insulin deficiency, rhabdomyolysis, hemolysis
Retention from drugs - ACE inhibitors, ARBs, NSAIDs, potassium-sparing diuretics, trimethoprim, heparin
Receipt of excess K⁺ - high K⁺ diet, blood transfusions, IV KCl
Rare: Addison's disease (↓ aldosterone), pseudohypoaldosteronism

Clinical Features:

Mild (5-6): Often asymptomatic
Moderate (6-7): Muscle weakness, fatigue
Severe (>7): Paralysis, arrhythmias, cardiac arrest

ECG Changes (in order of increasing severity):

Peaked/tall T waves (earliest)
Prolonged PR interval
Widened QRS
Sine wave pattern
Ventricular fibrillation / asystole

Treatment (Mnemonic: C BIG K Drop):

Step	Drug	Mechanism	Onset
C - Cardiac membrane stabilization	Calcium gluconate / CaCl₂	Stabilizes myocardium	1-3 min (temporary)
B - Beta-2 agonist	Salbutamol (albuterol) nebulization	Shifts K⁺ into cells	15-30 min
I - Insulin + glucose	Regular insulin + D50W	Shifts K⁺ into cells	15-30 min
G - (gut elimination)	Kayexalate (sodium polystyrene) or Patiromer	GI K⁺ exchange	Hours
K - Kidney / dialysis	Furosemide / Hemodialysis	Removes K⁺ from body	Hours
Drop - Lower total body K⁺	Dietary restriction, stop offending drugs	Prevention	Ongoing

NaHCO₃ (sodium bicarbonate) - corrects acidosis, shifts K⁺ intracellularly.

9. Urinary Tract Infection (UTI)

Definitions:

Bacteriuria: Bacteria in urine (may be asymptomatic)
Cystitis: Infection of bladder (lower UTI)
Pyelonephritis: Infection of kidney (upper UTI)
Complicated UTI: Structural/functional abnormality, immunocompromise, pregnancy, male patient, catheter-associated

Most common organism: Escherichia coli (80% of community-acquired UTIs). Also: Klebsiella, Proteus, Enterococcus, Staphylococcus saprophyticus (young sexually active women).

Epidemiology: More common in women (shorter urethra). UTI risk factors in women: sexual activity ("honeymoon cystitis"), diaphragm use, post-menopause. In men: BPH, urinary stasis.

Clinical Features:

Lower UTI (Cystitis)	Upper UTI (Pyelonephritis)
Dysuria, frequency, urgency	Fever (>38°C), chills
Suprapubic pain	Flank pain / CVA tenderness
Hematuria	Nausea/vomiting
No fever	May have cystitis symptoms

Diagnosis:

Dipstick: Positive leukocyte esterase and nitrites
Urinalysis: WBC >5/HPF (pyuria), bacteria
Culture: >10⁵ CFU/mL = significant bacteriuria
Urine culture with sensitivity guides antibiotic choice

Treatment:

Condition	First-line	Duration
Uncomplicated cystitis (women)	Nitrofurantoin, TMP-SMX, or Fosfomycin	3-7 days
Cystitis in men	TMP-SMX or Fluoroquinolone	7 days
Mild-moderate pyelonephritis (outpatient)	Oral fluoroquinolone (ciprofloxacin)	7-14 days
Severe pyelonephritis (inpatient)	IV ceftriaxone or piperacillin-tazobactam	14 days
Catheter-associated UTI	Based on culture; treat symptomatic only	7-14 days

Treat asymptomatic bacteriuria ONLY in: Pregnancy, before urological procedures.

Recurrent UTI prophylaxis: Post-coital antibiotics, low-dose nightly TMP-SMX, cranberry juice (weak evidence).

10. Polycystic Kidney Disease (PKD)

Two main types:

Feature	ADPKD (Autosomal Dominant)	ARPKD (Autosomal Recessive)
Inheritance	AD	AR
Gene	PKD1 (85%) - chr 16; PKD2 (15%) - chr 4	PKHD1 - chr 6
Protein	Polycystin-1, Polycystin-2	Fibrocystin
Onset	Adults (30-50 years)	Childhood/neonatal
Prognosis	ESKD by 5th-6th decade	Severe; often fatal in neonates

ADPKD - Key Features:

Multiple fluid-filled cysts in both kidneys → progressively enlarge
Kidneys become massively enlarged (palpable masses)
Symptoms: Flank pain, hematuria, hypertension (earliest symptom), abdominal fullness

Extrarenal Manifestations of ADPKD (tested frequently!):

Intracranial (Berry) aneurysms (~10-40%) - risk of subarachnoid hemorrhage → screen with MRA
Hepatic cysts (most common extrarenal finding)
Mitral valve prolapse (25%)
Colonic diverticula
Pancreatic cysts

Diagnosis:

Ultrasound: multiple bilateral renal cysts (Ravine criteria by age)
CT/MRI: better for small cysts and extrarenal manifestations

Complications:

Hypertension (earliest - RAAS activation)
Renal calculi (uric acid or calcium oxalate)
Cyst hemorrhage (hematuria)
Cyst infection (fever + flank pain + negative standard culture → treat with fluoroquinolones which penetrate cysts)
ESKD

Treatment:

Tolvaptan (vasopressin V2 receptor antagonist) - slows cyst growth, approved for rapidly progressing ADPKD; risk: hepatotoxicity
Antihypertensives: ACE inhibitors / ARBs
Adequate hydration (suppresses vasopressin)
Pain management
Dialysis/Transplant for ESKD
PD is preferred over HD in PKD (avoids heparin, reducing cyst/intracranial bleed risk)

Quick Reference Summary Table

Topic	Key Marker	Key Treatment
CKD	GFR <60 for ≥3 months	ACE/ARB, control BP, dialysis at Stage 5
AKI	SCr ↑ ≥0.3 in 48h	Treat cause; dialysis (AEIOU)
Nephrotic Syndrome	Proteinuria >3.5 g/day	Steroids (MCD); ACE/ARB for all
Nephritic Syndrome	RBC casts + hematuria	Treat underlying (PSGN = supportive)
Diabetic Nephropathy	Microalbuminuria (earliest)	SGLT2i + ACE/ARB + glycemic control
Dialysis	Kt/V adequacy	HD 3×/wk; PD daily
RFTs	eGFR best overall marker	CrCl by Cockcroft-Gault
Hyperkalemia	K⁺ >5.5 + peaked T waves	Calcium → Insulin/glucose → Remove
UTI	Dysuria + pyuria	Nitrofurantoin/TMP-SMX 3-7d
PKD	Bilateral cysts + Berry aneurysm	Tolvaptan, ACE/ARB

Sources: Textbook of Family Medicine 9e; Brenner and Rector's The Kidney; Comprehensive Clinical Nephrology 7th Ed; Campbell Walsh Wein Urology; National Kidney Foundation Primer on Kidney Diseases 8e

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