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KembaraXtra -Medicine- Nephritic Syndrome
Nephritic syndrome represents acute glomerulonephritis, an inflammatory injury of the glomeruli characterized by abrupt onset of hematuria, often cola- or coffee-colored, with or without red blood cell casts, variable proteinuria, reduced urine output, edema, hypertension, azotemia, and possible acute renal failure. The underlying mechanism is incompletely understood but involves immune-mediated injury to the glomerular basement membrane with crescent formation reflecting severe capillary wall damage.
Poststreptococcal glomerulonephritis is a classic cause and follows infection with group A β-hemolytic streptococci, occurring as a nonsuppurative complication after pharyngitis or skin infection. A latent period of 1–3 weeks after pharyngeal infection or 2–4 weeks after cutaneous infection helps distinguish it from IgA nephropathy. Immune complex deposition produces characteristic subepithelial “hump-shaped” deposits, with low complement C3 levels lasting 6–8 weeks. Prognosis is excellent in most patients, particularly children, with spontaneous recovery of renal function within weeks, although transient nephrotic features may occur during recovery.
Other infectious causes include sepsis, pneumonia, endocarditis, viral infections including HIV, and parasitic diseases such as malaria. Hepatitis virus–associated glomerular disease may present with nephritic or nephrotic features and typically shows persistently low complement levels. Noninfectious immune-mediated causes include systemic lupus erythematosus, Henoch–Schönlein purpura, vasculitis, Goodpasture syndrome, and IgA nephropathy, which is the most common cause worldwide and typically presents with hematuria coinciding with upper respiratory infections and normal complement levels.
Patients commonly present with hematuria, periorbital or generalized edema, hypertension, and symptoms related to recent infection. Children may develop facial edema, whereas older adults may present with congestive heart failure. Nonspecific symptoms such as malaise, anorexia, nausea, and weakness are common. Physical examination often reveals elevated blood pressure and fluid overload.
Evaluation centers on urinalysis showing hematuria, proteinuria, and red blood cell casts, which are diagnostic of active glomerular inflammation. Laboratory studies include complete blood count, renal function tests, serum albumin, complement levels, streptococcal antibody titers, and cultures when infection is suspected. Renal ultrasound assesses kidney size, and chest radiography may reveal pulmonary edema. Renal biopsy is not routinely required for poststreptococcal disease but is indicated for atypical features, persistent hypocomplementemia, severe proteinuria, or progressive renal dysfunction.
Management focuses on treating the underlying cause and controlling complications. Streptococcal infections are treated with appropriate antibiotics. Salt and fluid restriction, loop diuretics for edema, and antihypertensive therapy with ACE inhibitors or ARBs are used to control blood pressure and proteinuria. Severe cases with uremia, electrolyte disturbances, refractory fluid overload, or acidosis require hemodialysis. Hypertensive emergencies are managed with titratable intravenous antihypertensives.
Hospital admission is required for patients with oliguria, rising creatinine, significant edema, electrolyte abnormalities, severe hypertension, heart failure, or suspected systemic disease. Mild cases in otherwise healthy patients may be managed with close outpatient follow-up and nephrology referral. Prognosis is generally favorable, but long-term monitoring of blood pressure, renal function, and proteinuria is essential, particularly in IgA nephropathy and rapidly progressive forms.
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