Background: We assessed whether immunohistologic markers for glomerular or tubulointerstitial injury might provide better correlations with ongoing renal function and disease activity as compared with the WHO classification or the NIH activity and chronicity indices in lupus nephritis. Methods: Thirty-three patients with clinically defined systemic lupus underwent renal biopsy over a 1-year period at Hospital Loayza in Lima, Peru. Biopsy specimens were evaluated for macrophages, proliferating cells, α-actin expression, and type IV collagen deposition in both glomeruli and the tubulointerstitium and the results compared with the current WHO and NIH classifications in relation to the clinical presentation. Results: Patients with WHO class IV lupus nephritis were more likely to have lower serum complements, greater proteinuria and hematuria, and worse renal function. An elevated NIH activity index correlated with microhematuria, proteinuria, and impaired renal function, whereas an elevated chronicity index correlated with renal function, hypertension, and microhematuria, but not with proteinuria. The presence of glomerular macrophages correlated with both glomerular α-actin expression and type IV collagen deposition, but did not correlate with renal function or proteinuria. In contrast, interstitial macrophages correlated not only with interstitial collagen deposition and myofibroblast accumulation, but also correlated with both renal function and the presence of nephrotic syndrome. Conclusions: Both the WHO classification and the NIH activity/chronicity indices correlate with clinical manifestations of lupus nephritis. While glomerular macrophage accumulation correlates with mesangial cell activation (α-actin expression) and collagen deposition, and interstitial macrophage accumulation correlates with interstitial fibroblast activation and collagen deposition, only interstitial macrophages correlate with renal function. Of particular interest will be future studies to determine whether these markers correlate with the prognosis.

We report two similar cases of fracture and proximal migration of temporary femoral haemodialysis catheters. The two cases were encountered 6 years apart. These types of occurrences, especially in centres where catheter reuse is practiced, are not uncommon but seldom reported in the literature. Alert dialysis staff on both the occasions took remedial steps in time, which prevented embolisation of the catheters into the inferior vena cava. Both the catheters were removed successfully by the surgical team.

Microcytic anemia refractory to usual supplementation is an important clue to an alternative diagnosis. Accompanying pulmonary and renal involvement during the disease course suggests a multisystem disease. Small-vessel vasculitis should be suspected in any patient who presents with a multisystem disease that is not caused by an infectious or malignant process. Among these, antineutrophilic cytoplasmic antibodies (ANCA)-associated vasculitis is a distinct subclass involving anti-neutrophil cytoplasmic antibody (ANCA) as the common pathogenesis. Microscopic polyangiitis is a rare form of such vasculitis in children characterized by pulmonary-renal syndrome with pauci-imune rapidly progressive glomerulonephritis and a poor outcome.

SUMMARYWe describe a case of a 40-year-old lady diabetic and hypertensive, who presented with increasing fatigue and decreased physical endurance attributable to deterioration in renal function. The renal biopsy revealed drug-induced acute tubulointerstitial nephritis and the chronology of the events suggested the aetiology to be a recent intake of aceclofenac for knee pain. The patient improved with oral corticosteroids and the renal functions returned to baseline in 3 weeks. We did not come across a case of aceclofenac-induced acute tubulointerstitial nephritis on extensive electronic search of literature. This is probably the first case report of acute tubulointerstitial nephritis associated with the use of aceclofenac, a newer potent non-steroidal anti-inflammatory drug. BACKGROUND

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