[Differential diagnosis of chronic interstitial nephritis and primary chronic pyelonephritis].
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Acute tubulointerstitial nephritis (TIN) was diagnosed during a 10-year period in 6 previously healthy children (4 boys) with a mean age of 10 years (range 2.5-14 years). All presented with a non-specific history. First laboratory findings were nearly identical, with a raised erythrocyte sedimentation rate and non-oliguric renal failure; the urine contained protein, glucose, and leucocytes, but no bacteria. A serologically proven infection (streptococcal infection 2x; mononucleosis 1x) or drug-related TIN (penicillin) was present in 4 children; in one, both conditions could have been responsible. One girl suffered from idiopathic TIN with uveitis. Rapid progression of renal failure occurred in 3 children, but the response to steroid therapy was satisfactory. No dialysis was necessary and all patients showed a complete recovery. We think that acute TIN occurs more frequently than suggested previously. Many episodes are probably mild or subclinical and the rate of spontaneous remission is high. The results of initial laboratory evaluation in conjunction with acute renal failure and predominantly proximal tubular dysfunction, are sufficiently typical to arouse suspicion of acute TIN at an early stage, although they do not permit any conclusion as to the aetiology.
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We describe a patient with rheumatoid arthritis (RA) who developed hypersensitivity after 3 weeks of therapy with azathioprine with fever, jaundice and renal insufficiency. A percutaneous liver biopsy was compatible with hypersensitivity hepatitis. During azathioprine rechallenge, the symptoms recurred within a few days, consistent with the diagnosis of an acute hypersensitivity reaction. This report is the first to describe the association of an azathioprine induced hypersensitivity simultaneously involving the liver and the kidneys, in the same patient with RA, with resurgence after rechallenge.
Wegener's granulomatosis (WG) is a primary systemic vasculitis involving predominantly the upper and lower respiratory tracts and the kidneys. Few diseases can cause deterioration of renal function and progression to renal failure as rapidly as WG. We describe a woman with WG who developed rapid progression to renal failure within 10 days of starting azathioprine prescribed as maintenance therapy for vasculitis. Her renal biopsy showed acute tubulointerstitial nephritis and no active glomerulonephritis. This case illustrates the importance of the history and urine sediment in differentiating drug hypersensitivity from rapidly progressive glomerulonephritis in patients with WG.
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We report a case of sarcoid granulomatous tubulointerstitial nephritis diagnosed by renal biopsy. A 60-year-old man presented with productive cough, and exertional dyspnea of 3 months duration. A chest X-ray film revealed diffuse reticulonodular infiltrates in both lung fields. A transbronchial lung biopsy specimen showed inflammation of the alveolar septum associated with non-caseating granulomas. The patient also had tubular proteinuria and glucosuria. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in both lungs and kidneys. Renal function tests revealed tubular dysfunction. Tubulointerstitial nephropathy was suspected. A renal biopsy specimen exhibited tubulointerstitial nephritis associated with numerous non-caseating granulomas, similar to the findings of the lung biopsy specimen. No glomerular abnormalities were evident. Later, a scalene node biopsy confirmed the diagnosis of sarcoidosis. Prednisolone therapy yielded a favorable outcome for both the renal and pulmonary involvement. During the corticosteroid therapy, measurement of the urinary beta-2-microglobulin concentration proved a valuable monitoring tool for assessing the recovery of the tubular impairment.