Fasting in Ramadan is not associated with deterioration of chronic kidney disease: A prospective observational study.

Although not mandatory for patients, many Muslims fast in Ramadan. We aimed to investigate the effects of long hours (17.5) fasting on renal functions in patients with chronic kidney disease (CKD). Stage 3-5 CKD patients with stable renal function were recruited to this prospective observational study three months ahead of Ramadan in 2015. All patients were instructed regarding possible deleterious effects of dehydration caused by fasting. Forty-five patients (mean age 66.8 ± 10.3 years, 68.8% male) chose to fast and 49 (mean, age: 64.1 ± 12.6 years, 51% male) chose not to fast. Clinical and laboratory data were recorded before and after Ramadan. Baseline clinical and laboratory parameters were similar in the two groups, except for higher serum creatinine and lower estimated glomerular filtration rate (eGFR) in the nonfasting group (2.22 ± 0.99 vs. 1.64 ± 0.41 mg/dL, P <0.001 and 3 1.9 ± 12.4 vs. 42.6 ± 9.8 mL/min, P <0.001, respectively). More than 30% elevation in serum creatinine after Ramadan occurred in 8.8% and 8.1% of fasting and nonfasting patients, respectively (P = 0.9). More than 25% drop eGFR after Ramadan was noted in seven (15.5%) and six (12.2%) fasting and nonfasting patients, respectively (P = 0.642). Patients with ≥ 25% drop in eGFR (13 vs. 81) were older (72.3 ± 8.3 years vs. 64.3 ± 11.7 years, P = 0.020) and more frequently using diuretics (69.2% vs. 35.8%, P = 0.023). In multiple linear regression analysis, only advanced age was found to be associated with ≥25% drop in eGFR after Ramadan in the fasting group. Fasting during Ramadan was not associated with increased risk of declining in renal functions in patients with Stage 3-5 CKD. However, elderly patients may still be under a higher risk.

The protective effect of infliximab against carbon tetrachloride-induced acute lung injury.

OBJECTIVES: Carbon tetrachloride (CCl4) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl4 induced lung injury. MATERIALS AND METHODS: Rats were divided into control, CCl4, and CCl4+Ib groups. A single dose of 2 ml/kg CCI4 was administered to CCI4 group and a single dose of 7 mg/kg Ib was given to CCl4+Ib group 24 hr before applying CCI4. RESULTS: TNF-α, malondialdehyde (MDA), nitric oxide (NO) and caspase-3 levels of the CCl4 group were markedly higher than both the control and CCl4+Ib groups. The CCI4+Ib group had lower histopathological injury than the CCl4 group. CONCLUSION: Ib as a strong TNF-α blocker decreases the production of proinflammatory cytokines, MDA, and oxidative stress leading to a protective effect against CCl4 induced lung tissue injury.