NephrologyTier 2Disease (DEADMAN)

Tubulo-interstitial kidney disorders

Description

Disorders primarily affecting the renal tubules and interstitium, rather than the glomerulus - typically present with disproportionate tubular dysfunction (concentrating defect, electrolyte wasting) relative to the degree of GFR reduction, and a bland urine sediment (unlike glomerulonephritis)

Acute interstitial nephritis (AIN) is drug-induced in the majority of cases - a common cause of unexplained AKI, especially in hospitalised patients on multiple new medications
Chronic tubulointerstitial disease - analgesic nephropathy, reflux nephropathy, and obstructive uropathy are classic causes of chronic interstitial scarring

AIN - drug-induced (most common - antibiotics, especially beta-lactams and NSAIDs, PPIs), infection (pyelonephritis), autoimmune (Sjogren's, sarcoidosis, TINU syndrome) - a hypersensitivity/inflammatory infiltrate in the interstitium
Chronic tubulointerstitial disease - analgesic nephropathy (chronic NSAID/combination analgesic use -> papillary necrosis and cortical scarring), reflux nephropathy (recurrent childhood UTI + vesicoureteric reflux -> focal scarring), heavy metal/lithium toxicity, myeloma cast nephropathy

AIN: the classic triad (fever, rash, eosinophilia) is present in only a minority - do not rely on it; eosinophiluria supports but is neither sensitive nor specific; renal biopsy remains the definitive diagnosis when the cause is unclear
A bland urine sediment (no/minimal blood, no red cell casts, low-grade proteinuria) helps distinguish from glomerulonephritis
A careful medication history/timeline is often more diagnostically useful than any single test in suspected drug-induced AIN

Stop the offending drug - the single most important step in drug-induced AIN, often sufficient alone
Corticosteroids - considered for AIN if renal function fails to improve after stopping the drug, though the evidence for benefit is not definitive
Chronic tubulointerstitial disease - address the underlying cause (stop analgesics, correct reflux/obstruction); established fibrosis is not reversible

NSAID/antibiotic/PPI use, sarcoidosis, Sjogren's syndrome, TINU syndrome (tubulointerstitial nephritis + uveitis), myeloma, reflux nephropathy

Drug-induced AIN recognised and treated early often recovers substantially, though some patients are left with residual CKD
Chronic tubulointerstitial disease progresses insidiously and is frequently under-recognised until advanced, since it lacks the dramatic urinary findings of glomerular disease

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