Chronic interstitial nephritis lithium

Penicillins Proton pump inhibitors Chronic interstitial nephritis Cyclosporine Lithium Aristolochic acid Renal vasculitis, thrombosis, and cholesterol emboli ... 

Both lithium and demeclocycline have been reported to cause acute renal failure. Long-term lithium therapy may also cause chronic interstitial nephritis. 

Extensive literature has accumulated concerning other forms of renal dysfunction during long-term lithium therapy, including chronic interstitial nephritis and minimal-change glomerulopathy with nephrotic syndrome. Some instances of decreased glomerular filtration rate have been encountered but no instances of marked azotemia or renal failure. 

A 48-year-old man taking lithium and chlorprothixene had a creatinine clearance of 60 ml/minute and a renal biopsy showing chronic interstitial nephritis (380). 

Lithium, cyclosporine, and only a few other drugs have been reported to cause chronic interstitial nephritis, which is usually a progressive and irreversible lesion. Streptozotocin and other antineoplastic nitrosoureas also cause dose-dependent chronic interstitial disease. In addition, mesalazine, 5-aminosalicylic acid, and ifosfamide may cause chronic interstitial nephritis, which usually resolves promptly when drug use is discontinued. 

Symptomatic polyuria and polydipsia can be reversed by discontinuation of lithium therapy or ameliorated with amiloride or NSAIDs during continued lithium therapy (see Chap. 49). Acute renal failure is usually reversible with supportive care, including dialysis to reduce toxic blood lithium concentrations. Progressive chronic interstitial nephritis is treated by discontinuation of lithium therapy, adequate hydration, and avoidance of other nephrotoxic agents. 

Chronic interstitial nephritis Cyclosporine Lithium Aristolochic acid... 

The pathogenesis includes dehydration secondary to nephrogenic diabetes insipidus, as well as direct proximal and distal tubular cell toxicity resulting in ATN. Chronic tubulointerstitial nephritis attributed to lithium is evidenced most commonly by biopsy findings of interstitial fibrosis, tubular atrophy, and glomerular sclerosis (Presne et al. 2003 SUva 2004). The pathogenesis may involve cumulative direct lithium toxicity since duration of therapy has correlated with the decline in the GFR. The major risk factor for AKI is an elevated lithium concentration, particularly in associatimi with dehydration. 

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