Neurogenic Bladder and Acute Kidney Injury in Leukodystrophy.

Leukodystrophies are genetic white matter disorders. In the young, they represent an important cause of progressive neurological disability. Impairment of the bladder function may be part of the clinical picture of leukodystrophies. A neurogenic bladder is a dysfunctional urinary bladder caused by a disease of the central or peripheral nervous system involved in the control of micturition. In our patient, leukodystrophy-induced neurogenic bladder and acute kidney injury were revealed. If untreated, a neurogenic bladder can cause renal failure and urinary incontinence. Patients with a neurogenic bladder should be monitored, and management should aim to preserve renal function and achieve social continence.

Associations of platelet indices with proteinuria and chronic kidney disease.

OBJECTIVES: Platelet (PLT) indices are predictive in many diseases and conditions. The relationships of these indices with proteinuria and progression of renal disease are not well known. This study aimed to assess PLT indices in patients with primary glomerular nephrotic range proteinuria (PGNRP), with and without chronic kidney disease (CKD), and to compare these indices with those of healthy individuals (His). METHODS: This cross-sectional study was performed from January 2015 to May 2015. HIs (n = 57) and patients with PGNRP (n = 41) were enrolled. PLT indices and blood biochemistry parameters were compared between HIs and patients with PGNRP, as well as between subgroups of patients with PGNRP who had CKD (n = 23) and those who did not have CKD (n = 18). RESULTS: There were no statistically significant differences in any PLT indices (i.e., platelet number, mean platelet volume, plateletcrit, and platelet distribution width) between HIs and patients with PGNRP, or between the subgroups of patients with PGNRP. However, patients with PGNRP who had CKD exhibited higher median C-reactive protein and mean albumin levels, compared with patients who did not have CKD. CONCLUSIONS: Pathological processes in proteinuria and CKD are not associated with PLT indices.

Neurobrucellosis Presented by Cerebral Salt Wasting.

This case reported here was a 27-year-old female patient, and she had no chronic disease other than hypothyroidism. She was brought to the ER with complaints of fever, chills, weakness, and hyponatremia. She has been diagnosed with brucellosis using a serum tube agglutination test (STAT). Cerebrospinal fluid (CSF) analysis and brain MRI findings supported the central nervous system (CNS) involvement of the brucella. Despite intense 3% NaCl hydration, her hyponatremia was persisting. Sodium stabilized on the 14th day when the antibrucellosis treatment effect was settled. Hyponatremia was attributed to cerebral salt wasting (CSW) due to neurobrucellosis.

The effects of Mucuna pruriens on the renal oxidative stress and transcription factors in high-fructose-fed rats.

In the present study, we evaluated the effects of M. pruriens administration on metabolic parameters, oxidative stress and kidney nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling pathways in high-fructose fed rats. Male rats (n = 28) were divided into 4 groups as control, M. pruriens, fructose, and M. pruriens plus fructose. All rats were fed a standard diet supplemented or no supplemented with M. pruriens (200 mg/kg/d by gavage). Fructose was given in drinking water for 8 weeks. High fructose consumption led to an increase in the serum level of glucose, triglyceride, urea and renal malondialdehyde (MDA) levels. Although M. pruriens treatment reduced triglyceride and MDA levels, it did not affect other parameters. M. pruriens supplementation significantly decreased the expression of NF-Ò¡B and decreased expression of Nrf2 and HO-1 proteins in the kidney. This study showed that the adverse effects of high fructose were alleviated by M. pruriens supplementation via modulation of the expression of kidney nuclear transcription factors in rats fed high fructose diet.