Chronic Interstitial Nephritis



Distinct causes of chronic interstitial nephritis include analgesic abuse, heavy metal ingestion, and radiation exposure. Diabetes mellitus, mul­tiple myeloma, and essential hypertension, dis­eases that affect multiple organs, may also cause significant renal interstitial disease. No specific etiology is identifiable for up to one half of all cases of chronic interstitial nephritis. In each case the disease process may be wholly asymptomatic, with azotemia discovered incidentally on a lab­oratory screening panel. Hypertension is a regular feature of these disorders and can be the initial, presenting sign of renal disease. Sterile pyuria and microscopic hematuria are presenting signs in some patients. A large number of cases are rec­ognized only when end-stage renal failure occurs and a retrospective diagnosis is made based on a history of toxic exposure.

Analgesic nephropathy follows the ingestion over years of time of combination analgesics, usu­ally a salicylate plus either phenacetin or acetam­inophen. Use of the single agents alone is not as­sociated with renal injury. The lesion is first seen in the renal medulla and may reflect a toxic effect of acetaminophen that is intensified by medullary concentration. Salicylates appear to be permissive to the effect, perhaps by blocking production of vasodilator prostaglandins that support medul­lary blood flow. The disease process may be halted if analgesic intake is stopped early in the course.

Decreased urinary concentrating ability results from the medullary lesion, but frank polyuria is uncommon. Papillary necrosis, visible on renal radiography (IVP) and causing passage of tissue in the urine, is a hallmark of the disease. Treat­ment consists of withdrawing combination anal­gesic preparations, rigorously controlling blood pressure, and maintaining surveillance for uri­nary tract obstruction from sloughed papillary tis­sue.

Heavy metal nephropathy occurs chiefly with chronic lead ingestion, leaded paints and illicit alcohol being prominent sources. Aside from the coexistence of an anemia disproportionate to the degree of renal insufficiency, prominent periph­eral neuropathy, and a high incidence of gouty arthritis, lead nephropathy is clinically similar to analgesic nephropathy. Interstitial nephritis pre­viously attributed to urate deposition in the kid­ney (urate nephropathy) is now recognized to be lead nephropathy with saturnine gout. Increased urinary lead excretion following EDTA adminis­tration is a useful diagnostic test, but EDTA in­fusion may cause toxic renal failure and is not useful in treating this disorder.

Chronic radiation nephritis may follow some years after local retroperitoneal irradiation. It, too, is associated with progressive, often silent, renal insufficiency; accelerated hypertension is a com­mon complication. Proteinuria of modest propor­tion may be seen. There is no treatment for the nephropathy, but strict management of hyperten­sion is important.