Nephritis — inflammation and disorders of the kidneys

Types and parts affected

• Glomerulonephritis: inflammation primarily of the glomeruli; can be acute or chronic and often alters filtration and urine composition.
• Acute interstitial nephritis: inflammatory change in the interstitium and tubules, frequently drug-related or allergy-mediated.
• Pyelonephritis: infection-driven inflammation that typically involves renal pelvis and parenchyma, usually bacterial in origin.

Each type targets different anatomical structures and therefore produces characteristic laboratory and clinical findings. Clinicians distinguish acute presentations, which develop over days to weeks, from chronic nephritis, which evolves more slowly and may lead to progressive loss of kidney function.

Causes and mechanism

Common causes include infections (bacterial, viral, or post-infectious immune responses), autoimmune disorders that mistakenly target renal tissue, and exposure to toxins or certain medications. The inflammatory response may be mediated by antibodies, immune complexes, or cellular immune activity that damages capillary walls and tubular cells. Injury to glomerular structures can reduce blood flow through filters, impairing urine production and allowing blood cells or protein to cross into urine.

Signs, symptoms, and notable findings

• Changes in urine: blood in the urine (hematuria), foamy urine from protein, or reduced urine volume (oliguria).
• Retention of metabolic waste leading to symptoms described collectively as uremia, such as fatigue, nausea, and altered mental status in severe cases.
• Systemic features: swelling (edema), high blood pressure, fever in infective forms, and flank pain in pyelonephritis.

Diagnosis and management

Evaluation typically begins with urinalysis (to detect blood, protein, casts), blood chemistry (creatinine, electrolytes), and serologic tests for underlying autoimmune or infectious causes. Imaging (ultrasound or CT) can assess structural complications, and a renal biopsy is often required to define specific histologic patterns and guide therapy.

• Supportive care: blood pressure control, dietary adjustments, and management of fluid and electrolyte balance.
• Targeted treatment: antibiotics for bacterial infections; corticosteroids or other immunosuppressive agents for immune-mediated forms; discontinuation of offending drugs when relevant.
• Advanced cases: persistent or severe injury may require temporary dialysis or, in end-stage disease, long-term renal replacement therapy or transplantation.

Prognosis depends on the cause, the speed of diagnosis, and response to treatment. Some acute forms resolve completely, while chronic or recurrent inflammation may progress to chronic kidney disease. Historical advances—such as improved microscopy, serologic techniques, and the development of renal biopsy—have made diagnosis and targeted therapy more effective. Prevention emphasizes prompt treatment of urinary infections, cautious use of potentially nephrotoxic drugs, and control of systemic diseases that affect the kidneys such as diabetes and autoimmune conditions.

For further overview material on inflammatory processes and renal physiology, consult introductory resources and clinical guidelines that review diagnostic algorithms and treatment pathways in more detail (inflammation overview, clinical summaries at related sites).