Abstract
Isolated or predominant tubulointerstitial lupus nephritis is rare. Here we report the case of a thirty eight years old male who was diagnosed with systemic lupus erythematosus (SLE) according to clinical and laboratory criteria and presented with impaired renal function and non nephrotic range proteinuria. Renal biopsy revealed normal glomeruli but interstitial momonuclear cell infiltration. Immunohiostochemistry (IHC) showed immune deposits in the tubular basement membranes (TBMs), and the peritubular capillary basement membranes (PTCBMs). He was started on high dose oral steroids, which were gradually tapered over one month. His renal functions improved over few days and normalized by the end of the first month of treatment. He was continued on low dose steroids and azathioprine with no evidence of relapse. Predominant tubulointerstitial lupus can occur, although rarely; and it runs a favorable course with good response to treatment.
Highlights
Tubulointerstitial disease (TID) of the kidneys is a well recognized feature of lupus nephritis (LN), occurring in 66% of kidney biopsy specimens of patients with systemic lupus erythematosus (SLE)(1)
To the best of our knowledge only twelve cases had been reported[3]. This possibility should be suspected when a patient with SLE presents with a rising plasma creatinine concentration and a urinalysis that is relatively normal or shows only a few red cells and/or white cells. These changes may be accompanied by signs of tubular dysfunction such as metabolic acidosis due to type 1 renal tubular acidosis (RTA), hyperkalemia due to impaired distal potassium secretion, or hypokalemia due to salt-wasting and secondary hyperaldosteronism
Tubulointerstitial lesions may be encountered in all classes of lupus nephritis, but most commonly encountered in class IV lupus nephritis
Summary
Tubulointerstitial disease (TID) of the kidneys is a well recognized feature of lupus nephritis (LN), occurring in 66% of kidney biopsy specimens of patients with systemic lupus erythematosus (SLE)(1). To the best of our knowledge only twelve cases had been reported[3] This possibility should be suspected when a patient with SLE presents with a rising plasma creatinine concentration and a urinalysis that is relatively normal or shows only a few red cells and/or white cells. These changes may be accompanied by signs of tubular dysfunction such as metabolic acidosis due to type 1 (distal) renal tubular acidosis (RTA), hyperkalemia due to impaired distal potassium secretion, or hypokalemia due to salt-wasting and secondary hyperaldosteronism. The patient presented with impaired renal function, sub nephrotic proteinuria and evidence of tubular dysfunction
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