Although mild hyperuricemia is common in patients with renal disease, it has usually been considered a marker of reduced nephron mass rather than a risk factor for progression of kidney disease. On the other hand, experiments in a rat model demonstrated important deleterious effects of mild hyperuricemia on several aspects of renal structure and function. In the present investigation, the impact of the discontinuation of allopurinol therapy on the control of hypertension and the rate of progression of chronic kidney disease was considered. The present work involved 50 patients, suffering from stage 3 and 4 chronic kidney disease. All of them were on chronic allopurinol therapy for the treatment of mild hyperuricemia. Their blood pressure, serum creatinine and uric acid levels were followed for 12 months following allopurinol withdrawal. Urinary transforming growth factor beta-1 (TGF-β₁) was assayed by a solid-phase enzyme-linked immunosorbent assay. After allopurinol withdrawal, significant worsening of hypertension, significant acceleration of the rate of loss of kidney function and a significant increase in the urinary excretion of TGF-β₁ were observed in the group of patients who were not receiving pharmacological blockers of the renin-angiotensin system. In conclusion, asymptomatic hyperuricemia has a deleterious effect on the progression of chronic kidney disease and the control of hypertension. This effect was blocked by treatment with renin-angiotensin system blockers.

In a preliminary experiment, 38% of the spent dialysis fluid water was reclaimed by a forward osmosis process through a cellulose triacetate membrane. The simplicity of forward osmosis and its minimal external energy requirements may allow the construction of a small bulk device that can reclaim a considerable portion of the water used in the patient's dialysis process. For developing an acceptable ambulatory dialysis system, decreasing the bulk of the fluid and equipment carried on the patient is essential. Forward osmosis may feasibly be used for dialysis fluid regeneration in ambulatory dialysis systems.

Background: Hepatorenal syndrome (HRS) may result from decreased renal perfusion in advanced liver cirrhosis patients. Copeptin is co-secreted with the arginine vasopressin (AVP) and is increased in patients with decompensated liver cirrhosis, however, limited studies associated Copeptin with HRS.Objective: This study aimed to evaluate serum Copeptin as a predictor of HRS in advanced liver cirrhosis patients. Patients and Methods: A case-control study had been carried out on a total of 40 subjects divided into; Group 1: 20 decompensated cirrhotic patients with HRS, Group 2: 10 decompensated cirrhotic patients with normal kidney function, and Group 3: 10 healthy controls. The following had been made; history taking, clinical examination, laboratory investigations: complete blood picture, liver function tests, coagulation profile, serum sodium, and creatinine. Serum Copeptin was measured using an enzyme-linked immunosorbent assay (ELISA). Results: Serum Copeptin levels; mean ±SD in pmol/L were significantly increased in group 1 (HRS) (7.3±1.11) compared to group 2 (3.6±0.99) and group 3 (2.3±0.31) (P˂0.001). Serum Copeptin levels positively correlated with serum creatinine, prothrombin time, total bilirubin (P˂0.05), and negatively correlated with serum albumin (P˂0.05), and sodium (P˂0.001), with no correlation with other parameters. The receiver operating characteristic (ROC) curve for serum Copeptin validity as a predictor of HRS in advanced liver cirrhosis patients, at a cutoff of 3.99 pmol/L showed 95.1% sensitivity, 70.2% specificity, and 85.1% accuracy. Conclusion: Serum Copeptin may predict HRS in advanced liver cirrhosis with high sensitivity and specificity.