Acute kidney injury associated to sulfamethoxazole urine crystal: The importance of clinical suspicion.

Management of acute kidney injury (AKI) associated with drug-induced crystal nephropathy can be difficult, and timely diagnosis is critical to resolve this condition. We present the case of a 55-year-old woman with history of systemic lupus erythematosus (SLE), who, after treatment with trimethoprim/sulfamethoxazole (TMP/SMX) for suspected Pneumocystis jirovecii pneumonia, developed severe AKI. Automated urinary sediment initially reported hematuria, leukocyturia and "uric acid crystals". She did not have allergic symptoms, clinical manifestations of active SLE nor hyperuricemia. AKI persisted despite volume expansion with crystalloids. Due to SMX exposure, it was suspected that "uric acid crystals" could be in reality "SMX crystals", and were a possible cause of crystal nephropathy. TMP/SMX was withheld and urinary alkalization was performed, with subsequent resolution of AKI. SMX urine crystals were posteriorly confirmed by Fourier transform infrared spectroscopy.

Diagnosis of light chain cast nephropathy through immunostaining of the urine: Perfecting the "liquid biopsy".

Light chain (LC) cast nephropathy is the main cause of kidney injury and an important determinant of poor survival in patients with multiple myeloma (MM). It is usually suspected when an MM patient with elevated serum concentration of free LC presents kidney failure, but it often requires confirmation by kidney biopsy. We report the case of a 73-year-old woman who presented with fatigue, weight loss, and constipation. Laboratory exams revealed anemia, hypercalcemia, and kidney failure. Urine sediment analysis demonstrated irregular crystalline "waxy type" casts. With the hypothesis of LC cast nephropathy, immunostaining of the urine sediment was performed. The analysis revealed several rectangular and irregular casts with intense and bright stain for λ LCs only. A myelogram was performed, showing extensive occupation of the bone marrow by plasma cells; and immunofixation in urine and serum revealed monoclonal IgG-λ component, confirming the diagnosis of IgG-λ MM. This case highlights the potential utility of the urine sediment analysis and immuno-staining as a reliable non-invasive alternative method for diagnosis of cast nephropathy in patients with monoclonal gammopathies.

Prevention of liver ischemia reperfusion injury by a combined thyroid hormone and fish oil protocol.

Several preconditioning strategies are used to prevent ischemia-reperfusion (IR) liver injury, a deleterious condition associated with tissue resection, transplantation or trauma. Although thyroid hormone (T3) administration exerts significant protection against liver IR injury in the rat, its clinical application is controversial due to possible adverse effects. Considering that prevention of liver IR injury has also been achieved by n-3 polyunsaturated fatty acid (n-3 PUFA) supplementation to rats, we studied the effect of n-3 PUFA dietary supplementation plus a lower dose of T3 against IR injury. Male Sprague-Dawley rats receiving fish oil (300 mg/kg) for 3 days followed by a single intraperitoneal dose of 0.05 mg T3/kg were subjected to 1 h of ischemia followed by 20 h of reperfusion. Parameters of liver injury (serum transaminases, histology) and oxidative stress (liver contents of GSH and oxidized proteins) were correlated with fatty acid composition, NF-κB activity, and tumor necrosis factor-α (TNF-α) and haptoglobin expression. IR significantly modified liver histology; enhanced serum transaminases, TNF-α response or liver oxidative stress; and decreased liver NF-κB activity and haptoglobin expression. Although IR injury was not prevented by either n-3 PUFA supplementation or T3 administration, substantial decrease in liver injury and oxidative stress was achieved by the combined protocol, which also led to increased liver n-3 PUFA content and decreased n-6/n-3 PUFA ratios, with recovery of NF-κB activity and TNF-α and haptoglobin expression. Prevention of liver IR injury achieved by a combined protocol of T3 and n-3 PUFA supplementation may represent a novel noninvasive preconditioning strategy with potential clinical application.