Nephritic syndrome: an overview
Nephritic syndrome (glomerulonephritis) presents with hematuria carrying dysmorphic erythrocytes or erythrocyte casts, often with hypertension, edema, and reduced GFR, spanning a spectrum from isolated microscopic hematuria to rapidly progressive glomerulonephritis (RPGN) with over 50% GFR loss in days to weeks. Kidney biopsy with immunofluorescence and serology (ANCA, anti-GBM, complement, antinuclear antibody) identifies the cause, and any RPGN pattern is a nephrology emergency requiring urgent biopsy and, for pauci-immune or anti-GBM disease, immediate high-dose immunosuppression.
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What this article covers
- Overview
A clinical syndrome spanning mild to catastrophic: nephritic syndrome, also termed glomerulonephritis, ranges from asymptomatic microscopic hematuria to the most severe form, rapidly progressive…
- Epidemiology
RPGN etiology is dominated by three diseases: ANCA-associated glomerulonephritis, lupus nephritis, and anti-glomerular basement membrane (anti-GBM) antibody disease account for the most common causes…
- Risk factors
Recent upper respiratory infection or physical exertion: classic trigger for the recurrent gross hematuria of IgA nephropathy.
- Pathophysiology
Glomerular capillary wall inflammation, not simple protein leak, defines the syndrome: immune injury to the glomerular capillary wall produces both leakage of erythrocytes (hematuria) and reduced…
- Clinical features
Hematuria with dysmorphic erythrocytes or erythrocyte casts is the defining feature, distinguishing glomerular bleeding from other urinary tract sources of blood.
- Differential diagnosis
Nephrotic syndrome: distinguished by nephrotic-range proteinuria, hypoalbuminemia, and hypercholesterolemia as the dominant picture rather than hematuria with dysmorphic erythrocytes or casts; see nephrotic-syndrome-an-overview.
- Diagnosis
The diagnosis of glomerulonephritis is traditionally made by kidney biopsy, which categorizes the disease by immunofluorescence pattern (linear, granular, or pauci-immune) and by complement level…
- Management
First, control blood pressure and volume in every patient: lisinopril, start 2.5-5 mg PO daily titrated to the maximal tolerated dose (or losartan 50-100 mg PO daily), plus furosemide 20-80 mg PO…
- Complications
Progression to end-stage kidney disease: the dominant long-term risk, most severe with untreated RPGN, which reaches dialysis dependence within days to weeks if untreated.
- Prognosis
Prognosis depends heavily on both the specific etiology and the time to treatment: early treatment of RPGN can reverse lesions, while delay allows progression to dialysis dependence within days to weeks.
- Prevention
Treat streptococcal skin and throat infections promptly to reduce the risk of poststreptococcal glomerulonephritis, though treatment after infection is established does not reliably prevent the nephritic complication.
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Related articles
- Approach to hematuria
Hematuria is present in urine when at least 3 erythrocytes per high-power field are seen on microscopy, and the first branch point is glomerular versus nonglomerular bleeding, based on erythrocyte morphology and casts. Gross hematuria always requires urologic evaluation and cystoscopy, asymptomatic microscopic hematuria is risk-stratified by American Urological Association criteria to select repeat testing, imaging, or cystoscopy, and glomerular hematuria is treated with disease-specific immunosuppression after biopsy.
- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Chronic kidney disease
Chronic kidney disease is abnormal kidney structure or function present for more than 3 months, staged by the Kidney Disease: Improving Global Outcomes (KDIGO) system using estimated glomerular filtration rate and albuminuria, and managed with blood pressure control, renin-angiotensin blockade, an SGLT2 inhibitor, and correction of its metabolic complications.
- Membranoproliferative glomerulonephritis
Membranoproliferative glomerulonephritis is a rare chronic glomerulonephritis divided into immune-complex forms, most often driven by hepatitis C virus infection, and complement-mediated C3 glomerulopathies from alternative-pathway dysregulation, diagnosed by kidney biopsy with immunofluorescence. Treatment targets the underlying cause plus immunosuppression for nephrotic-range proteinuria or kidney dysfunction, and more than half of patients progress to end-stage kidney disease within 15 years.