Annual cardiovascular mortality in patients with chronic kidney disease (CKD) is much higher than in the general population. The rate of sudden cardiac death increases as the stage of CKD increases and could be responsible for 60% of cardiac deaths in patients undergoing dialysis. In hemodialysis units treating patients with CKD, cardiac arrest occurs at a rate of seven arrests per 100,000 hemodialysis sessions. Important risk factors for sudden cardiac death in patients with CKD include hospitalization within the past 30 days, a drop of 30 mmHg in systolic blood pressure during hemodialysis, duration of life on hemodialysis, time since the previous dialysis session, and the presence of concomitant diabetes mellitus. As a result of the adverse cardiomyopathic and vasculopathic milieu in CKD, the occurrence of arrhythmias, conduction abnormalities, and sudden cardiac death could be exacerbated by electrolyte shifts, divalent ion abnormalities, diabetes, sympathetic overactivity, in addition to inflammation and perhaps iron deposition. Impaired baroreflex effectiveness and sensitivity, as well as obstructive sleep apnea, might also contribute to the risk of sudden death in CKD. The likelihood of survival following cardiac arrest is very low in dialysis patients. Primary and secondary prevention of cardiac arrest could reduce cardiovascular mortality in patients with CKD. Cardioverter-defibrillator implantation decreases the risk of sudden death in patients with CKD. The decision to implant a cardioverter-defibrillator should be influenced by the patient's age and stage of CKD.

The kidney and heart have essential roles in maintaining blood volume homeostasis and in the regulation of systemic blood pressure. Acute or chronic dysfunction in either the heart or kidneys can induce dysfunction in the other organ, resulting in the so-called cardiorenal syndromes, which are classified into five different types. Abrupt worsening of cardiac function predisposes an individual to acute kidney injury from renal hypoperfusion or renal congestion. Progressive, sometimes permanent, chronic kidney impairment can result from chronic renal hypoperfusion or congestion. Heart failure is common in patients with acute kidney injury. Chronic kidney disease predisposes individuals to atherosclerotic, arteriosclerotic and cardiomyopathic disease. Finally, both cardiac and renal disease can also occur secondary to systemic conditions, such as diabetes or autoimmune disease. This Review examines the mechanisms presiding over the first four types of cardiorenal syndromes. These mechanisms provide a template that accounts for the heart-kidney interactions that occur in patients whose concomitant cardiac and renal conditions result from a third cause.

Proteinuria is a common problem encountered in the treatment of renal transplant recipients, occurring in up to 45% of patients. Proteinuria from native kidneys falls rapidly after renal transplantation, and persistent or worsening proteinuria is usually indicative of allograft pathology. Biopsy studies of transplant patients with proteinuria have confirmed that transplant-specific diagnoses (transplant glomerulopathy, interstitial fibrosis and tubular atrophy, and acute rejection) are more commonly found than other proteinuric conditions, such as glomerulonephritis. As in the nontransplant setting, proteinuria is associated with worse clinical outcomes, including an increased risk for death, cardiovascular events, and graft loss. Blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers will reduce proteinuria, but the long-term effect of these medications on patient and graft survival remains unknown.

Cognitive dysfunction is reportedly highly prevalent among chronic kidney disease (CKD) patients. A variety of screening tools and neuropsychiatric batteries are used to quantify the magnitude and nature of this dysfunction. Our objective is to summarize the neurocognitive testing used, and determine what degree cognitive dysfunction is reported in CKD patients. All study designs published in English that contained participants who were either pre‐dialysis patients, haemodialysis (HD) or peritoneal dialysis (PD) patients or renal transplant recipients were considered. Reported comparative non‐CKD control data was also collected. All study designs were included. The search period encompassed articles from 1980 to May 2018. This review is registered with PROSPERO (CRD42018096568). Of the 1711 articles screened, 148 articles were relevant and used in the meta‐analysis. Commonly used assessments were The Mini–Mental State Examination (MMSE), The Modified Mini–Mental State Examination, the Trails Making Tests (TMT) forms A and B and components of the Wechsler Adult Intelligence Scale: Digit Span and Digit Symbol. Means for all assessments were adjusted using a random effects model to account for the differences in variance. Adjusted mean MMSE scores were significantly lower for both pre‐dialysis (26.08, n = 17 073) and HD (26.31, n = 3314) patients when compared to non‐CKD controls (28.21, n = 5226). PD (58.01 s, n = 859) and HD (56.04 s, n = 2344) patients also took significantly longer to complete the Trails Making Task A than non‐CKD controls (37.62 s, n = 4809). Patients with CKD, especially pre‐dialysis and those requiring dialysis, are likely to exhibit impairments in cognition that can be identified with specific screening neuropsychological assessments.

Nephrogenic systemic fibrosis (NSF), previously known as nephrogenic fibrosing dermopathy, is a generalized fibrotic disorder occurring in people with renal failure, following exposure to gadolinium-based contrast agents used to enhance MRI. The cellular elements involved in pathology of NSF include bone-marrow-derived collagen-producing fibrocytes, myofibroblasts and activated macrophages. Mechanisms that have been hypothesized to play a role in the pathogenesis of NSF include upregulation of osteopontin, imbalance between matrix metalloproteinases and tissue inhibitor of metalloproteinase 1, and presence of transforming growth factor-β, nuclear factor κB, decorin and metallothioneins. Gadolinium (both free and chelated) is thought to be a bioactive trigger for NSF. Elucidation of these potential pathomechanisms would be useful for development of targeted therapies for NSF.

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Background: Bone mineral density (BMD) decreases postrenal transplantation. Evidence demonstrating the effects of bisphosphonates on BMD and fracture risk beyond 1-year posttransplant is sparse in existing literature, but remains essential to enhance clinical outcomes in this population. Objective: Our study aimed to systematically review and meta-analyze the current literature on the use of any bisphosphonate in the adult renal transplant population beyond the first year of renal transplant to determine its effect on BMD and fracture incidence. Design: We conducted a systematic review and meta-analysis of primary research literature that included full-text, English-language, original randomized clinical trials (RCTs) and observational studies. Setting: Patient data were primarily captured in an outpatient setting across various studies. Patients: Our population of interest was patients older than 18 years who received deceased/living donor kidney transplantation and any bisphosphonate with a follow-up greater than 12 months posttransplantation. Measurements: The primary outcome was change in BMD from baseline. Secondary outcomes were the incidence of fractures and effects of other confounders on bone health. Methods: We included RCTs and observational studies that satisfied our inclusion criteria. Each study was analyzed for risk of bias and data were extrapolated to analyze for overall statistical significance accounting for heterogeneity of studies. Results: Sixteen studies (N = 1762) were analyzed. The follow-up ranged from 12 to 98 months. There was a nonsignificant improvement in BMD with bisphosphonate treatment persisting into the second and third years posttransplant at the lumbar spine. The calculated standardized mean BMD difference was −0.29 (−0.75 to 0.17), P = .22. Only 5 studies reported a total of 43 new fractures. Prednisone ( P < .01), low body weight ( P < .001), low body mass index ( P < .01), and male gender ( P < .05) correlated with reduced lumbar and femoral BMD. Limitations: Limitations of this review include the use of BMD as a surrogate outcome, the bias of the included studies, and the incomplete reporting data in numerous analyzed studies. Conclusions: We demonstrate no statistically significant benefit of bisphosphonate treatment on BMD beyond the first year postrenal transplantation. Despite heterogeneity of treatment, a differential nonsignificant improvement in lumbar spine BMD was consistent and may be clinically relevant. Trial Registration: PROSPERO CRD42019125593

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