Diabetic nephropathy (DN) is a major healthcare challenge. It occurs in up to 50% of those living with diabetes, is a major cause of end‐stage kidney disease (ESKD) that requires treatment with dialysis or renal transplantation, and is associated with significantly increased cardiovascular morbidity and mortality. DN is a clinical syndrome characterized by persistent albuminuria and a progressive decline in renal function, but it is increasingly recognized that the presentation and clinical course of kidney disease in diabetes is heterogeneous. The term diabetic kidney disease (DKD) is now commonly used to encompass the spectrum of people with diabetes who have either albuminuria or reductions in renal function. In this article, the clinical presentation and approach to diagnosis of DKD will be discussed, as will its prognosis. The general principles of management of DKD will also be reviewed with reference to current international guidelines.

Background and objectives: Hemodialysis (HD)-induced myocardial stunning driven by ischemia is a recognized complication of HD, which can be ameliorated by HD techniques that improve hemodynamics. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD may initiate and drive the same process. In this study, we examined the prevalence and associations of HD-induced repetitive myocardial injury and long-term effects on LV function and patient outcomes. Design, setting, participants, & measurements: Seventy prevalent HD patients were assessed for evidence of subclinical myocardial injury at baseline using serial echocardiography and followed up after 12 mo. Intradialytic blood pressure, hematologic and biochemical samples, and patient demographics were also collected at both time points. Results: Sixty-four percent of patients had significant myocardial stunning during HD. Age, ultrafiltration volumes, intradialytic hypotension, and cardiac troponin-T (cTnT) levels were independent determinants associated with its presence. Myocardial stunning was associated with increased relative mortality at 12 mo (P = 0.019). Cox regression analysis showed increased hazard of death in patients with myocardial stunning and elevated cTnT than in patients with elevated cTnT alone (P < 0.02). Patients with myocardial stunning who survived 12 mo had significantly lower LV ejection fractions at rest and on HD (P < 0.001). Conclusions: HD-induced myocardial stunning is common, and may contribute to the development of heart failure and increased mortality in HD patients. Enhanced understanding of dialysis-induced cardiac injury may provide novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.

Background and objectives: Hemodialysis is associated with hemodynamic instability, acute cardiac ischemia, and the development of regional wall motion abnormalities (RWMAs). This study used serial intradialytic H₂¹⁵O positron emission tomography scanning to confirm that the development of dialysis-induced RWMAs was associated with reduction in myocardial blood flow (MBF). Design, setting, participants, & measurements: Four prevalent hemodialysis patients without angiographically significant coronary artery disease had measurements of MBF during standard hemodialysis and biofeedback dialysis. All patients underwent serial measurements of MBF using positron emission tomography. Concurrent echocardiography was used to assess left ventricular function and the development of RWMAs. Hemodynamic variables were measured using continuous pulse wave analysis. Results: Mean prehemodialysis MBF was within the normal range. Global MBF was acutely reduced during hemodialysis. Segmental MBF was reduced to a significantly greater extent in areas that developed RWMAs compared with those that did not. Not all regions with reduced MBF were functionally affected, but a reduction in myocardial blood flow of >30% from baseline was significantly associated with the development of RWMAs. No significant differences in hemodynamic tolerability, RWMA development, or MBF between dialysis modalities were observed. Conclusions: Hemodialysis is associated with repetitive myocardial ischemia, which, in the absence of coronary artery disease, may be due to coronary microvascular dysfunction. Stress-induced segmental left ventricular dysfunction correlates with matched reduction in MBF. Functional poststress recovery is consistent with myocardial stunning induced by hemodialysis. This process may be important in the development of heart failure in long-term hemodialysis patients.

Background and objectives: Hemodialysis (HD)-induced regional wall motion abnormalities (RWMAs) are common in HD patients and driven by ischemia. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD-induced myocardial ischemia may initiate the same process. We examined the effect of HD-induced repetitive myocardial stunning on global and regional LV function. Design, setting, participants & measurements: We analyzed data from 30 patients, previously identified as developing HD-induced myocardial ischemia. Serial echocardiographic assessments of global and regional LV performance were performed at baseline and repeated after 12 mo. Results: Several patients developed segments with a fixed reduction in systolic function of >60% after 1 yr. In this patient group, there was a significant reduction in resting LV ejection fraction (EF) from 61.5 ± 10.1% to 52.9 ± 8.6% (P < 0.007). Peak LV EF in response to dialysis also decreased from 59.5 ± 10% versus 49.9 ± 6.5% (P < 0.003), with a consequent increase in HD-induced hypotension (P < 0.0001). Conclusions: HD-induced myocardial stunning may progress over 12 mo to the development of regional fixed systolic dysfunction, consistent with underlying myocardial hibernation and fibrosis. This may be an important and potentially modifiable process in the development of heart failure in HD patients.

Summary: Background and objectives: Many patients with AKI are cared for by non-nephrologists. This can result in variable standards of care that contribute to poor outcomes. Design, setting, participants, & measurements: To improve AKI recognition, a real-time, hospital-wide, electronic reporting system was designed based on current Acute Kidney Injury Network criteria. This system allowed prospective data collection on AKI incidence and outcomes such as mortality rate, length of hospital stay, and renal recovery. The setting was a 1139-bed teaching hospital with a tertiary referral nephrology unit. Results: An electronic reporting system was successfully introduced into clinical practice (false positive rate, 1.7%; false negative rate, 0.2%). The results showed that there were 3202 AKI episodes in 2619 patients during the 9-month study period (5.4% of hospital admissions). The in-hospital mortality rate was 23.8% and increased with more severe AKI (16.1% for stage 1 AKI versus 36.1% for stage 3) (P<0.001). More severe AKI was associated with longer length of hospital stay for stage 1 (8 days; interquartile range, 13) versus 11 days for stage 3 (interquartile range, 16) (P<0.001) and reduced chance of renal recovery (80.0% in stage 1 AKI versus 58.8% in stage 3) (P<0.001). Utility of the Acute Kidney Injury Network criteria was reduced in those with pre-existing CKD. Conclusions: AKI is common in hospitalized patients and is associated with very poor outcomes. The successful implementation of electronic alert systems to aid early recognition of AKI across all acute specialties is one strategy that may help raise standards of care.