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Renal stimulation tests document the dynamic response of the glomerular filtration rate (GFR) after a single or a combination of stimuli, such as an intravenous infusion of dopamine or amino acids or an oral protein meal. The increment of the GFR above the unstimulated state has formerly been called the renal functional reserve (RFR). Although the concept of a renal reserve capacity has not withstood scientific scrutiny, the literature documenting renal stimulation merits renewed interest. An absent or a blunted response of the GFR after a stimulus indicates lost or diseased nephrons. This information is valuable in preventing, diagnosing and prognosticating acute kidney injury and pregnancy-related renal events as well as chronic kidney disease. However, before renal function testing is universally practiced, some shortcomings must be addressed. First, a common nomenclature should be decided upon. The expression of RFR should be replaced by renal functional response. Second, a simple protocol must be developed and propagated. Third, we suggest designing prospective studies linking a defective stimulatory response to emergence of renal injury biomarkers, to histological or morphological renal abnormalities and to adverse renal outcomes in different renal syndromes.

Aims. AKI is common after cardiac surgery involving CPB. S-cystatin C is a novel early biomarker for AKI awaiting validation in this setting. Goal was to develop a clinical predictive model for AKI and test the added value of s-cystatin C within the first 24 hrs post-op. Methods. 259 patients were enrolled. Patients with severe pre-existing renal insufficiency were excluded (eGFR

This review discusses renal sodium handling in heart failure. Increased sodium avidity and tendency to extracellular volume overload, i.e. congestion, are hallmark features of the heart failure syndrome. Particularly in the case of concomitant renal dysfunction, the kidneys often fail to elicit potent natriuresis. Yet, assessment of renal function is generally performed by measuring serum creatinine, which has inherent limitations as a biomarker for the glomerular filtration rate (GFR). Moreover, glomerular filtration only represents part of the nephron's function. Alterations in the fractional reabsorptive rate of sodium are at least equally important in emerging therapy-refractory congestion. Indeed, renal blood flow decreases before the GFR is affected in congestive heart failure. The resulting increased filtration fraction changes Starling forces in peritubular capillaries, which drive sodium reabsorption in the proximal tubules. Congestion further stimulates this process by augmenting renal lymph flow. Consequently, fractional sodium reabsorption in the proximal tubules is significantly increased, limiting sodium delivery to the distal nephron. Orthosympathetic activation probably plays a pivotal role in those deranged intrarenal haemodynamics, which ultimately enhance diuretic resistance, stimulate neurohumoral activation with aldosterone breakthrough, and compromise the counter-regulatory function of natriuretic peptides. Recent evidence even suggests that intrinsic renal derangements might impair natriuresis early on, before clinical congestion or neurohumoral activation are evident. This represents a paradigm shift in heart failure pathophysiology, as it suggests that renal dysfunction-although not by conventional GFR measurements-is driving disease progression. In this respect, a better understanding of renal sodium handling in congestive heart failure is crucial to achieve more tailored decongestive therapy, while preserving renal function.

Acute kidney injury (AKI) remains a common complication after cardiopulmonary bypass (CPB) and can be diagnosed by serum creatinine. However, serum creatinine is an insensitive and nonspecific biomarker. This study was designed to investigate whether a correlation exists between urinary oxygen tension (UOT) and early markers of AKI. The aim was to evaluate whether UOT could provide warning signs of an insufficient renal oxygen supply, which can lead to postoperative AKI. Publication of this supplement has been supported by ISICEM.

Background: The novel urinary biomarkers for the early detection of kidney injury after ischemic or toxic insults have recently been well studied, including neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), cystatin C (Cys-C)and Nacetyl- β Dglucosaminidase (NAG). The lack of reference values have greatly impeded progress in the diagnosis and treatment of patients with AKI and have a detrimental effect on the possibly outcomes of clinical trials of cardiac surgery. Objective: The first objective of this study was to estimate the normal value of urinary NGAL, KIM-1, Cys-C and NAG in a healthy population. The second objective was to evaluate the diagnostic performance of urinary biomarkers in a prospective pilot study including adults after cardiopulmonary bypass (CPB) surgery. Methods: The age study population consist of 337 healthy non-smoking subjects (191 female, 146 male ranging from 4 months to 90 years). Urine samples were obtained at routine visit to the ZOL hospital. ELISA was used to measure urinary NGAL, KIM-1 and Cys-C. BIOQuant N-acetyl-B-D-Glucosaminidase (NAG) assay was used to measure NAG. The prospective pilot study consists of 25 adults (7 females, 18 males ranging from 51 to 84 years) who required CPB surgery. Urine and blood samples were obtained before and 3, 6, 12 and 24 hours after CPB surgery. Patients were divided into the AKI and non-AKI groups according to developed AKI after surgery, AKI was defined as a ≥ 0.3 mg/dl increase in sCr from the base line within 48h after the surgery. Urinary KIM-1 and NGAL were measured using ELISA assay. Results: Age study: significant age related differences were found for KIM-1, NGAL, Cys- C and NAG. In addition, significant differences between gender were found for KIM-1, NGAL and NAG. Cardiac study: 25 patients were enrolled, 20% developed AKI. Urinary KIM-1/Cr level was significantly increased 24h post surgery and was significantly associated with AKI within 24h ,while urinary NGAL level did not show such a performance. Conclusions: Based on our results, further study in larger population with biomarker panel is needed for the evaluation of normal values with variance factors as well as to establish the prediction value to diagnose AKI for long and short outcomes after cardiac surgery.