Chronic tubulointerstitial nephritis

Chronic tubulointerstitial nephritis (CTIN) is a pattern of kidney disease characterized by chronic inflammation and fibrosis of the tubulointerstitium (tubules and interstitial space) with relative preservation of glomeruli. Causative mechanisms: (1) Drug toxicity (NSAIDs—most common cause of CTIN; aminoglycosides, ACE inhibitors in renal artery stenosis, lithium); (2) Infection (reflux nephropathy from vesicoureteral reflux, recurrent pyelonephritis, TB); (3) Obstruction (kidney stones, BPH, malignancy)—leads to tubulointerstitial inflammation and fibrosis if prolonged; (4) Metabolic (hypercalcemia, hyperuricemia, hypokalemia); (5) Autoimmune (tubulointerstitial nephritis and uveitis syndrome—TINU, IgA nephropathy, SLE); (6) Idiopathic. Pathophysiology: initial injury (drug, infection, obstruction) triggers inflammatory cytokine release, tubular epithelial cell apoptosis, and fibroblast activation, leading to interstitial fibrosis and tubular atrophy. Unlike acute tubulointerstitial nephritis (acute kidney injury from drug allergy), CTIN develops insidiously over months to years. Presentation: asymptomatic (detected by routine labs showing elevated creatinine and/or proteinuria), or symptomatic with anemia, hypertension (from renin release), and progressive renal failure. Urinalysis shows pyuria (white blood cells) without significant proteinuria (< 1 g/day, distinguishing from glomerulonephritis which has heavy proteinuria). Imaging (ultrasound) may show small kidneys or scarring. Kidney biopsy (rarely needed) shows interstitial fibrosis and tubular atrophy with mononuclear inflammation. Diagnosis: clinical context (NSAID use, reflux history) + labs (non-nephrotic proteinuria, pyuria, normal complement levels). Management: identify and eliminate causative agent (stop NSAID, drain obstruction), treat underlying condition (reflux prophylaxis, metabolic correction), and manage complications (anemia, hypertension, CKD progression with ACE inhibitor/ARB). Prognosis depends on severity and whether causative factors are removed; established CTIN with fibrosis is often progressive to ESRD.