No abstract

The prevalence of chronic kidney disease (CKD) is increasing worldwide. The best therapies currently available focus on the control of blood pressure and optimization of renin-angiotensin-aldosterone system blockade. Currently available agents are only partially effective against hard end points such as the development of end-stage renal disease and are not discussed in this Review. Many other agents have been shown to reduce proteinuria and delay progression in animal models of CKD. Some of these agents, including tranilast, sulodexide, thiazolidinediones, pentoxifylline, and inhibitors of advanced glycation end-products and protein kinase C, have been tested to a limited extent in humans. A small number of randomized controlled human trials of these agents have used surrogate markers such as proteinuria as end points rather than hard end points such as end-stage renal disease or doubling of serum creatinine level. Emerging therapies that specifically target and reverse pathological hallmarks of CKD such as inflammation, fibrosis and atrophy are needed to reduce the burden of this chronic disease and its associated morbidity. This Review examines the evidence for emerging pharmacological strategies for slowing the progression of CKD.

In patients with autosomal dominant polycystic kidney disease (ADPKD), drinking more water could potentially reduce urine osmolality and suppress arginine vasopressin release and decrease the rate of kidney cyst growth and its associated organ dysfunction. In a 3-year trial, adults with ADPKD randomized to drink more water so as to lower urine osmolality did not have slower kidney growth than did a group who drank water as they wished.

Aim To compare the performance of the Nanra and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation for estimating glomerular filtration rate in pregnancy against the 24 h urine creatinine clearance. Methods Pregnant women had 24 h urine collections with simultaneous serum creatinine levels. Measured 24 h urine creatinine clearance was compared to two equations: Nanra and CKD-EPI. Level of concordance was measured, with an a priori bias acceptance of ±15 ml/min/1.73 m2. Results A total of 53 synchronous urine and serum creatinine samples were analysed. The Nanra equation had a bias of −13.4 ml/min/1.73 m2 while the CKD-EPI equation had bias of 14.2 ml/min/1.73 m2. Both equations showed a high degree of proportional error and had poor agreement with 24 h urine creatinine clearance. Conclusions None of the equations were shown to reliably measure the estimated glomerular filtration rate in pregnant women. A valid serum creatinine-based estimated glomerular filtration rate equation in pregnancy is yet to be established.