Renal disorders encompass a wide spectrum of conditions affecting kidney structure and function. The kidneys are essential for filtration of waste products, electrolyte and acid-base balance, blood pressure regulation, and hormone production. This article provides comprehensive coverage of major renal conditions.
Acute Kidney Injury (AKI)
| Parameter | Detail |
|---|---|
| Definition | Abrupt (within hours to days) decrease in kidney function, resulting in accumulation of waste products (creatinine, BUN) and dysregulation of fluid/electrolytes |
| Diagnostic criteria (KDIGO) | Increase in SCr by >=0.3 mg/dL within 48 hours, or increase to >=1.5x baseline within 7 days, or urine volume <0.5 mL/kg/h for 6 hours |
| Incidence | 15-20% of hospitalized patients; 30-50% of ICU patients |
AKI Classification (KDIGO Staging)
| Stage | Serum Creatinine | Urine Output |
|---|---|---|
| 1 | 1.5-1.9x baseline OR >=0.3 mg/dL increase | <0.5 mL/kg/h for 6-12 hours |
| 2 | 2.0-2.9x baseline | <0.5 mL/kg/h for >=12 hours |
| 3 | 3.0x baseline OR >=4.0 mg/dL increase OR initiation of RRT OR in patients <18 years, eGFR <35 mL/min/1.73m2 | <0.3 mL/kg/h for >=24 hours OR anuria for >=12 hours |
Prerenal vs Intrinsic vs Postrenal AKI
| Feature | Prerenal AKI | Intrinsic AKI (ATN) | Postrenal AKI |
|---|---|---|---|
| Cause | Hypoperfusion (hypovolemia, hypotension, decreased cardiac output, renal vasoconstriction) | Direct renal parenchymal damage (ischemic ATN, nephrotoxin ATN, acute interstitial nephritis, glomerulonephritis) | Obstruction of urinary tract (BPH, stones, tumors, neurogenic bladder, retroperitoneal fibrosis) |
| Most common subtype | 40-60% of AKI | 30-50% of AKI (ATN most common intrinsic) | 5-10% of AKI |
| Urinalysis | Normal or hyaline casts | Muddy brown granular casts, renal tubular epithelial cells (ATN); WBC casts, eosinophils (AIN); RBC casts (GN) | Normal or hematuria/pyuria |
| FeNa (fractional excretion of sodium) | <1% | >2% (ATN) | >2% (post-obstructive diuresis) |
| FeUrea | <35% | >50% | Variable |
| BUN:Creatinine ratio | >20:1 | <15:1 | Variable |
| Urine osmolality | >500 mOsm/kg | <350 mOsm/kg | Variable |
| Renal ultrasound | Normal | Normal or enlarged kidneys | Hydronephrosis, hydroureter |
| Response to fluids | Improves | No improvement | No improvement (relief of obstruction may improve) |
AKI Management
| Category | Prerenal | Intrinsic (ATN) | Postrenal |
|---|---|---|---|
| Immediate | Restore perfusion (IV fluids for hypovolemia, vasopressors for distributive shock, treat heart failure for cardiogenic) | Identify and remove cause (discontinue nephrotoxins, treat infection, manage contrast-induced AKI) | Relieve obstruction (Foley catheter, nephrostomy, ureteral stent) |
| Fluid management | NS or balanced crystalloids (LR, Plasmalyte); reassess volume status frequently | Euvolemia: maintenance IVF; Hypervolemia: diuretics (furosemide) | Maintain euvolemia post-obstruction |
| Monitoring | UOP, SCr, BUN, electrolytes, volume status | UOP, SCr, BUN, electrolytes, acid-base | UOP, SCr, post-obstruction diuresis |
| Dialysis indications | Refractory hyperkalemia, severe acidosis, volume overload unresponsive to diuretics, uremic complications (pericarditis, encephalopathy), severe toxin/drug overdose | Same | Same (if obstruction cannot be relieved or after relief if persistent) |
| Prevention | Avoid nephrotoxins, optimize volume status, consider holding ACEi/ARB during volume depletion | Low threshold for stopping NSAIDs, adjust drug dosing for renal function, avoid contrast if possible, use acetylcysteine for contrast nephropathy | Prompt relief of obstruction |
Chronic Kidney Disease (CKD)
| Parameter | Detail |
|---|---|
| Definition | Abnormalities of kidney structure or function present for >3 months with implications for health |
| Global prevalence | 10-15% of adults; affects >800 million worldwide |
| Most common causes | Diabetes (40-50%), hypertension (25-30%), glomerulonephritis (10-15%), other (polycystic kidney disease, interstitial nephritis, reflux nephropathy) |
CKD Staging (KDIGO)
| Stage | GFR (mL/min/1.73m2) | Description | Prevalence (US) |
|---|---|---|---|
| G1 | >=90 | Normal or high GFR with kidney damage (e.g., albuminuria) | 15-20% |
| G2 | 60-89 | Mildly decreased GFR with kidney damage | 25-30% |
| G3a | 45-59 | Mildly to moderately decreased GFR | 20-25% |
| G3b | 30-44 | Moderately to severely decreased GFR | 10-15% |
| G4 | 15-29 | Severely decreased GFR | 5-10% |
| G5 | <15 | Kidney failure (ESRD) | 1-2% |
Albuminuria Categories (KDIGO)
| Category | AER (mg/24h) | ACR (mg/g) | Description |
|---|---|---|---|
| A1 | <30 | <30 | Normal to mildly increased |
| A2 | 30-300 | 30-300 | Moderately increased (microalbuminuria) |
| A3 | >300 | >300 | Severely increased (macroalbuminuria) |
CKD Complications by Stage
| Complication | Screening | Onset (GFR threshold) | Management |
|---|---|---|---|
| Anemia | CBC | <30 mL/min (G4) | Iron supplementation, erythropoiesis-stimulating agents (ESAs) - target Hb 10-11.5 g/dL |
| Mineral and bone disorder (CKD-MBD) | Ca, Phos, PTH, vitamin D, ALP | <45 mL/min (G3b) | Phosphate binders (calcium-based, sevelamer, lanthanum, calcium-free binders), active vitamin D (calcitriol, paricalcitol), calcimimetics (cinacalcet) |
| Metabolic acidosis | Serum bicarbonate | <45 mL/min | Sodium bicarbonate supplementation (target HCO3 >=22 mEq/L) |
| Hyperkalemia | Serum potassium | <30 mL/min (or earlier with medications) | Dietary K restriction, avoid K-sparing diuretics/RAASi, potassium binders (patiromer, sodium zirconium cyclosilicate) |
| Volume overload | Clinical assessment | Variable | Dietary Na restriction, diuretics (loop diuretics preferred in CKD 4-5) |
| Cardiovascular disease | BP, lipids, ECG | All CKD stages | BP control (ACEi/ARB first-line), statins, antiplatelet therapy (secondary prevention) |
| Malnutrition | Albumin, prealbumin, nPNA | <30 mL/min (G4-G5) | Dietary counseling, adequate protein intake (0.8-1.0 g/kg/day), consider essential amino acids |
CKD Progression Slowing
| Intervention | Mechanism | Target | Evidence |
|---|---|---|---|
| ACEi/ARB | Reduce intraglomerular pressure, antifibrotic | Use maximum tolerated dose | Strong (reduces proteinuria, slows GFR decline) |
| SGLT2 inhibitors | Reduce intraglomerular pressure, metabolic effects | Dapagliflozin, empagliflozin, canagliflozin | Strong (DAPA-CKD, CREDENCE, EMPA-KIDNEY) |
| GLP-1 receptor agonists | Metabolic, anti-inflammatory, weight loss | Semaglutide | Moderate (FLOW trial) |
| Finerenone (ns-MRA) | Anti-inflammatory, antifibrotic | Mineralocorticoid receptor antagonist | Strong (FIDELIO-DKD, FIGARO-DKD) |
| BP control | Reduce hemodynamic injury | <130/80 mmHg | Strong |
| Glycemic control | Reduce glucotoxicity | HbA1c <7% (individualized) | Strong (microvascular) |
| Dietary protein restriction | Reduce hyperfiltration | 0.6-0.8 g/kg/day | Moderate (slows progression) |
| Avoid nephrotoxins | Prevent additional injury | Avoid NSAIDs, contrast (when possible), nephrotoxic medications | Strong |
| Smoking cessation | Vascular protection | Stop all tobacco | Strong |
| Sodium restriction | BP + volume control | <2 g/day (5 g salt) | Moderate |
CKD Risk Equation for Progression
The Kidney Failure Risk Equation (KFRE) uses age, sex, eGFR, and albuminuria to predict progression to kidney failure at 2 and 5 years.
| KFRE Risk Category | 2-Year Risk of ESRD | Management Focus |
|---|---|---|
| Low (<1% per year) | <5% | Monitoring, cardiovascular risk reduction |
| Moderate (1-2.5% per year) | 5-15% | Optimize RAASi, SGLT2i, lifestyle |
| High (2.5-5% per year) | 15-30% | Nephrology referral, prepare for RRT education |
| Very high (>5% per year) | >30% | RRT planning (fistula creation, transplant evaluation) |
Glomerulonephritis (GN)
Classification of GN by Presentation
| Syndrome | Presentation | Common Causes |
|---|---|---|
| Nephritic syndrome | Hematuria (RBC casts), hypertension, oliguria, mild proteinuria (<3.5 g/day), elevated BUN/Cr, periorbital/leg edema | Post-streptococcal GN, IgA nephropathy, lupus nephritis, anti-GBM disease, ANCA-associated GN |
| Nephrotic syndrome | Proteinuria >3.5 g/day, hypoalbuminemia, hyperlipidemia, edema, lipiduria | Minimal change disease, FSGS, membranous nephropathy, membranoproliferative GN, diabetic nephropathy, amyloidosis |
| Rapidly progressive GN (RPGN) | Rapidly declining GFR (>50% loss in 3 months), active urine sediment (RBC casts), crescent formation on biopsy | Anti-GBM disease (Goodpasture), ANCA vasculitis (GPA, MPA), lupus nephritis (class IV), post-infectious GN |
| Asymptomatic hematuria/proteinuria | Abnormal urinalysis without symptoms | IgA nephropathy (most common), thin basement membrane nephropathy, Alport syndrome |
| Chronic GN | Slowly progressive CKD over years | All types of chronic GN, hypertensive nephrosclerosis |
Common Glomerular Diseases
| Disease | Presentation | Age | Light Microscopy | Immunofluorescence | EM | Lab Findings | Treatment |
|---|---|---|---|---|---|---|---|
| IgA nephropathy (Berger disease) | Nephritic: hematuria (episodic, post-URI), +/- mild proteinuria | Young adults | Mesangial hypercellularity, matrix expansion | Mesangial IgA (dominant), C3, IgG (variable) | Mesangial electron-dense deposits | Normal C3, +/- elevated IgA | BP control, ACEi/ARB; fish oil, steroids if proteinuria >1 g/day, immunosuppression for RPGN |
| Membranous nephropathy | Nephrotic syndrome | Adults 40-60 | Diffuse GBM thickening (spikes on silver stain), no hypercellularity | Granular IgG (diffuse, GBM), C3, PLA2R | Subepithelial electron-dense deposits | Anti-PLA2R antibodies (70-80%), low C3 (25%) | ACEi/ARB, immunosuppression (cyclophosphamide + steroids, rituximab, calcineurin inhibitors) if progressive |
| Minimal change disease | Nephrotic syndrome (acute onset, severe) | Children (peak 2-6) | Normal light microscopy | Negative | Diffuse foot process effacement | Normal C3, normal renal function | Prednisone (90% respond), calcineurin inhibitors if steroid-dependent |
| FSGS (focal segmental glomerulosclerosis) | Nephrotic syndrome or proteinuria | Adults (variable) | Segmental sclerosis (collapsing, cellular, tip, perihilar variants) | IgM, C3 (segmental, non-specific) | Foot process effacement, GBM collapse | Normal C3 | ACEi/ARB, high-dose steroids for primary, calcineurin inhibitors, avoid secondary causes (HIV, obesity, heroin, genetic) |
| Lupus nephritis | Variable (class I-VI) | Women 15-45 | Variable by WHO/ISN class | Full house (IgG, IgA, IgM, C3, C1q) | Subendothelial, subepithelial, mesangial deposits | Positive ANA, anti-dsDNA, low C3/C4 | See SLE treatment section |
| ANCA vasculitis (GPA, MPA) | RPGN, pulmonary-renal syndrome | Adults >50 | Pauci-immune crescentic GN | Negative (pauci-immune) | No immune deposits | Positive ANCA (c-ANCA + PR3 in GPA; p-ANCA + MPO in MPA) | High-dose steroids + cyclophosphamide or rituximab |
| Anti-GBM disease (Goodpasture) | RPGN, pulmonary hemorrhage | Young adults (male) or elderly | Crescentic GN | Linear IgG along GBM | No immune deposits | Positive anti-GBM antibodies | Plasmapheresis + steroids + cyclophosphamide |
ISN/RPS Classification of Lupus Nephritis
| Class | Description | Frequency | Treatment |
|---|---|---|---|
| I | Minimal mesangial | Rare | No specific Rx |
| II | Mesangial proliferative | 10-15% | HCQ, +/- steroids |
| III | Focal (<50% glomeruli) | 20-25% | Steroids + MMF or cyclophosphamide |
| IV | Diffuse (>50% glomeruli) | 40-50% | Steroids + MMF or cyclophosphamide (induction), MMF or azathioprine (maintenance) |
| V | Membranous | 10-20% | ACEi/ARB; steroids + calcineurin inhibitor or MMF if nephrotic |
| VI | Advanced sclerosing | Rare | Conservative CKD management |
Nephrotic Syndrome
| Feature | Detail |
|---|---|
| Definition | Proteinuria >3.5 g/24h (or spot UPCR >3.5), hypoalbuminemia (<3.0 g/dL), edema, hyperlipidemia, lipiduria |
| Pathophysiology | Increased glomerular permeability to plasma proteins -> massive proteinuria -> hypoalbuminemia -> decreased oncotic pressure -> edema; hepatic lipoprotein synthesis stimulated -> hyperlipidemia |
| Complications | Infection (spontaneous bacterial peritonitis, cellulitis - loss of IgG/alternative pathway complement), thrombosis (renal vein, DVT, PE - loss of antithrombin III, protein C/S), hyperlipidemia (accelerated atherosclerosis), AKI, malnutrition |
Nephrotic Syndrome Treatment
| Intervention | Detail |
|---|---|
| Sodium restriction | <2 g/day |
| Diuretics | Loop diuretics (furosemide, torsemide), thiazides (synergistic) for edema |
| ACEi/ARB | Reduce proteinuria (antiproteinuric effect independent of BP) |
| Statins | Treat hyperlipidemia |
| Anticoagulation | Consider for severe hypoalbuminemia (<2.0 g/dL), especially if additional risk factors |
| Disease-specific treatment | Corticosteroids/immunosuppression per underlying etiology |
Kidney Stones (Nephrolithiasis)
| Type | Frequency | Causes | Radio-opaque | Urine pH | Treatment/Prevention |
|---|---|---|---|---|---|
| Calcium oxalate | 60-70% | Hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria | Yes | No specific | Increase fluid >2.5 L/day, dietary Na restriction, moderate Ca intake (not low Ca), thiazides (for hypercalciuria), potassium citrate (for hypocitraturia/hyperuricosuria) |
| Calcium phosphate | 10-15% | Hypercalciuria, RTA (type 1), hyperparathyroidism | Yes | Alkaline | Same as CaOx + treat underlying cause |
| Uric acid | 10-15% | Low urine pH (insulin resistance, metabolic syndrome), hyperuricosuria (high purine diet, gout, tumor lysis) | Radiolucent | Low (<5.5) | Urine alkalinization (K-citrate, NaHCO3), allopurinol (if hyperuricosuria), low purine diet |
| Struvite (magnesium ammonium phosphate) | 10-15% | Urease-producing bacteria (Proteus, Klebsiella, Ureaplasma) -> infection stones (staghorn calculi) | Yes | Alkaline | Complete stone removal (PCNL, ESWL, combined), eradicate infection, antibiotics, acetohydroxamic acid |
| Cystine | 1-2% | Cystinuria (autosomal recessive defect in dibasic amino acid transport) | Yes (faint) | Acidic | High fluid intake, urine alkalinization, tiopronin or penicillamine (thiol-binding drugs) |
Acute Stone Management
| Phase | Intervention |
|---|---|
| Pain control | NSAIDs (ketorolac, ibuprofen - first-line), opioids if severe |
| Conservative | Stones <5 mm: high likelihood of spontaneous passage (within 4 weeks); alpha-blockers (tamsulosin) for distal ureteral stones >5 mm (medical expulsive therapy) |
| Surgical intervention | Indications: stones >10 mm, failed medical therapy, obstruction with infection, AKI, solitary kidney, persistent pain, high-grade obstruction |
| Surgical options | ESWL (shock wave lithotripsy), ureteroscopy (URS) with laser lithotripsy, PCNL (percutaneous nephrolithotomy - for large/complex stones, especially staghorn) |
End-Stage Renal Disease (ESRD) and Dialysis
| Parameter | Detail |
|---|---|
| Definition | eGFR <15 mL/min/1.73m2 (CKD G5) requiring renal replacement therapy (dialysis or transplantation) to sustain life |
| ESRD incidence | ~130,000 new patients/year in US |
| ESRD prevalence | ~800,000 patients in US (70% on dialysis, 30% with transplant) |
Dialysis Modalities
| Feature | Hemodialysis (HD) | Peritoneal Dialysis (PD) |
|---|---|---|
| Principle | Blood circulates through extracorporeal circuit with dialyzer (artificial kidney); diffusion + convection | Peritoneal membrane acts as semipermeable membrane; dialysate instilled into peritoneal cavity |
| Access | AV fistula (gold standard), AV graft, tunneled dialysis catheter | Peritoneal catheter (Tenckhoff) |
| Location | In-center (3x/week, 4 hours/session), home HD (4-6x/week, 2-4 hours) | Home (CAPD: 4 exchanges/day, 2-3L each; CCPD: automated cycler at night) |
| Vascular access | Needle insertion into fistula/graft each session | No vascular access needed |
| Anticoagulation | Heparin (systemic or regional) during HD | Not required |
| Solute clearance | Higher efficiency per session | Lower efficiency but continuous |
| Fluid removal | Rapid (over 4 hours) | Slow and continuous (gentler) |
| Dietary restrictions | Strict: K, Na, Phos, fluid | Less strict: K, Na, Phos (some loss in PD), no fluid restriction as strict |
| Advantages | Efficient, professional care, social contact | Flexibility, independence, easier employment, hemodynamic stability (better for CV patients) |
| Disadvantages | Vascular access complications, dietary restrictions, travel limitations, hemodynamic instability | Catheter-related infections (peritonitis, exit site), metabolic complications, limited in patients with prior abdominal surgery/obesity |
| Contraindications | Severe hemodynamic instability | Prior abdominal surgery, adhesions, obesity, abdominal wall issues, severe COPD, non-compliance |
| Patient preference | M-F with transportation/support | Motivated, organized, good hygiene, home space |
Kidney Transplantation
| Feature | Detail |
|---|---|
| Donor types | Deceased donor (DDKT, ~60%), Living donor (LDKT, ~40%: related or unrelated) |
| Survival benefit | LDKT > DDKT > Dialysis; 5-year patient survival: LDKT 90%, DDKT 85%, Dialysis 40-50% |
| Evaluation | ABO compatibility, HLA matching, crossmatch, PRA, donor and recipient medical/surgical evaluation, psychosocial assessment |
| Immunosuppression | Induction (thymoglobulin, basiliximab) + Maintenance (tacrolimus + mycophenolate + corticosteroids) |
| Complications | Rejection (hyperacute, acute, chronic), infection (CMV, BK virus, PCP, UTI), malignancy (skin cancer, PTLD), CV disease, post-transplant diabetes |