Continuous renal replacement therapy (CRRT) remains the dominant form of renal support among critically ill patients worldwide. Current clinical practice on CRRT prescription mostly relies on high quality studies suggesting no impact of CRRT dose on critically ill patients' outcomes. Recent clinical practice guidelines have been developed based on these studies recommending a static prescribed CRRT dose of 20-25 ml/kg/h. There is a rationale for renewed attention to CRRT prescription/practice based on the concept of dynamic solute control adapted to the changing clinical needs of critically ill patients. In response, Acute Disease Quality Initiative convened a 17th consensus meeting centered on re-evaluation of CRRT. This work group developed 4 themes focused specifically on CRRT dose prescription, delivery and solute control that were summarized in a series of consensus statements, along with the identification of critical knowledge gaps. CRRT dose prescription and delivery can be based on effluent flow rate. Delivered dose should be routinely monitored to ensure coherence with prescribed dose. CRRT dose should be dynamic, in recognition of between- and within-patient variation in targeted solute control or unintended solute clearance. Quality measures specific for monitoring delivered CRRT dose have been proposed that require further validation, prior to implementation, into the practice of guiding optimal CRRT dosage.

The prevalence of hypertension in chronic kidney disease (CKD) patients exceeds that of the general population. Uncontrolled hypertension plays a significant role in progression to end stage renal disease and results in increased cardiovascular morbidity and mortality. A complex interplay between various pathophysiologic mechanisms is responsible for the development of hypertension in this patient population. The major factors being extracellular volume overload, increased endothelin-1 release and excess renin-angiotensin-aldosterone system and sympathetic nervous system activity. Dietary and lifestyle modifications have synergistic effects to drug therapy in the control of hypertension. There is no single blood pressure target that is optimal for all CKD patients. It is important to individualize the treatment depending on age, the severity of albuminuria, and comorbidities. Drugs blocking the renin-angiotensin-aldosterone system are the recommended first-line antihypertensive agents for most CKD patients. Intradialytic hypertension may be prevented by individualizing the dialysis prescription and using nondialyzable antihypertensives. New onset of hypertension in the elderly or new onset of difficult to control hypertension in a previously well controlled hypertensive patient should prompt the work up for atherosclerotic renal vascular disease.

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease worldwide. Sodium-glucose-linked transporter 2 (SGLT2) inhibitors are a new and promising class of antidiabetic agents that target renal tubular glucose reabsorption. Their action is based on the blockage of SGLT2 sodiumglucose cotransporters that are located at the luminal membrane of tubular cells of the proximal convoluted tubule (PCT), inducing glucosuria. It has been proven that they significantly reduce glycated hemoglobin (HbA1c), along with fasting and postprandial plasma glucose in patients with type II diabetes mellitus (T2DM). Glomerular hyperfiltration is a potential risk factor for DN. The SGLT2 inhibitors reduce sodium reabsorption in the proximal tubule, causing, through tubuloglomerular feedback (TGF), afferent arteriole vasoconstriction and reduction in hyperfiltration. The SGLT2 inhibitors reduced glomerular hyperfiltration in patients with T1DM, and in patients with T2DM, they caused transient acute reductions in glomerular filtration rate (GFR), followed by a progressive recovery and stabilization of renal function. Interestingly, recent studies consistently demonstrated a reduction in albuminuria. Recently, it was demonstrated that empagliflozin presents a significant cardioprotective effect. Although the SGLT2 inhibitors' efficacy is affected by renal function, new data have been presented that some SGLT2 inhibitors, even in mild and moderate renal impairments, induce significant HbA1c reduction. Although these data are promising, only dedicated renal outcome trials will clarify whether SGLT2 inhibitors, in addition to their glycemic and blood pressure (BP) benefits, may provide nephroprotective effects.