Syndecan‐1 belongs to the syndecan family of cell surface transmembrane heparan‐sulfate proteoglycans, which participate in cell proliferation, cell migration and cell‐matrix interactions. Decreased expression of syndecan‐1 has been observed in some gastrointestinal malignancies, and it is thought that high levels of syndecan‐1 correlate with the maintenance of epithelial morphology and inhibition of invasiveness. In our study, we characterized the expression of syndecan‐1 in normal, chronic pancreatitis and primary and metastatic human pancreatic cancer tissues, in cultured pancreatic cancer cell lines and in esophageal, gastric, colon, and liver cancers. Pancreatic cancer cell lines expressed syndecan‐1 mRNA and protein at variable levels. In addition, these cells also released syndecan‐1 into the culture medium. Pancreatic cancer tissues markedly over‐expressed syndecan‐1 mRNA in comparison with both chronic pancreatitis (2.4‐fold increase, p < 0.01) and normal pancreatic samples (10.6‐fold increase, p < 0.01). There was no difference in syndecan‐1 mRNA expression between early and advanced tumors. By in situ hybridization and immunohistochemistry, syndecan‐1 expression was evident at relatively low levels in the ductal cells and less frequently in acinar cells of the normal pancreas. In chronic pancreatitis, syndecan‐1 was present at low to moderate levels in areas with atrophic acinar cells and ductular complexes. In contrast, in pancreatic cancer tissues, syndecan‐1 was present at moderate to high levels in the majority of the cancer cells within the tumor mass and also in metastatic lesions of pancreatic tumors. Syndecan‐1 mRNA levels in other gastrointestinal malignancies (esophageal, gastric, colon and liver cancers) were not significantly different from the levels observed in the corresponding normal samples. Together, our findings suggest that syndecan‐1 expression by pancreatic cancer cells may be of importance in the pathobiology of this disorder and that its role in pancreatic cancer seems to be different from that in other gastrointestinal malignancies. Int. J. Cancer 88:12–20, 2000. © 2000 Wiley‐Liss, Inc.

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To our knowledge, this report was the first available study of the equipment and human resources utilized for RRT in AKI patients in Latin America.

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Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used by patients all over the world. Five to eighteen percent of the patients who receive NSAIDs can suffer from kidney-related side effects. Among them, the most relevant are sodium and water retention, hyponatremia, worsening of hypertension or preexisting cardiac failure, hyperkalemia, acute kidney injury, chronic kidney disease, papillary necrosis, nephrotic syndrome (NS), and acute interstitial nephritis. We report the case of a 65-year-old woman who developed acute tubular necrosis and NS a few days after receiving 15 mg of meloxicam (MLX) for 3 days for tendinitis. Steroid therapy was begun with normalization of kidney function after 7 weeks of treatment. NS (minimal change disease) was characterized by frequent remissions and relapses as prednisone was lowered under 30 mg/day. Azathioprine (100 mg/day) was added on the fifth month of diagnosis and a complete remission was finally obtained 4 years after hospital admittance. In her last medical checkup, 8 years after her debut and receiving azathioprine (50 mg) and prednisone (5 mg/day), renal function was normal (creatinine 1.0 mg/dL and creatinine clearance 80 mL/min/1.73 m 2 ), proteinuria was 150 mg/day and there was no hematuria or hypertension. The aim of communicating this case is to raise a warning about these renal side effects of MLX. After thorough review of literature, only one other report with the same findings was found.

Collapsing glomerulopathy is a form of focal segmental glomerulosclerosis that is usually associated with HIV-1 infection, and is characterized by its poor prognosis and almost inevitable progression to end-stage renal disease. Its pathological features include collapsed glomeruli, podocyte hypertrophy and hyperplasia, and pseudocrescents. This case report shows the evolution of a 58-year-old patient with non-HIV idiopathic collapsing glomerulopathy who presented with severe nephrotic syndrome and renal insufficiency and was treated with lisinopril and deflazacort, a synthetic corticosteroid that has shown fewer cosmetic effects and glucose and bone metabolism complications than prednisone. The patient responded with full recovery of renal function and normal range of protein excreted in urine after less than two years of treatment. The patient has not suffered a recurrence of his nephrotic syndrome after three years of steroid withdrawal. There is no proven therapy for collapsing glomerulopathy, and this case highlights an alternative for treating this disease with few secondary effects.

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We report a 28-year-old male with a hereditary nephritis (Alport (Rev Med Chile 2013; 141: 519-524).