Agbasi, Nneoma

In the cognate nephrology literature, a few recent publications from major academic centers in the United States have suggested that the incidence of contrast nephropathy was exaggerated and overstated. These investigators have concluded that intravenous contrast material administration was not associated with an increased risk of acute kidney injury (AKI), emergent dialysis, and short-term mortality in a cohort of patients with diminished renal function. As a contrarian opinion, we first describe a clear cut case of contrast-nephropathy resulting in AKI requiring hemodialysis treatment managed in the Renal Unit of the Mayo Clinic Health System, Northwestern Wisconsin, in the Spring of 2017. We subsequently revisit the overwhelming evidence-base in the English literature that supports the enormous impact of contrast-nephropathy as a clinical syndrome. We finally posit that these recent repudiations of the existence and significance of contrast-nephropathy as a significant clinical entity represent an overreach in statistical expertise. There is no basis for a requiem song over contrast-nephropathy

AbstractIntroduction: We first described the syndrome of rapid onset end stage renal disease (SORO‐ESRD), acute yet irreversible renal failure, in 2010.Objective: The impact of SORO‐ESRD renal allograft survival remains speculative and we plan to study this question.Methods: A retrospective analysis of individual adult patient‐level serum creatinine trajectories of ESRD patients on maintenance hemodialysis for >90 days at Mayo Clinic, Rochester, 2001–2013.Results: Of 1461 ESRD patients, 149 (10%) patients including 13 renal transplant recipients (RTRs) satisfied the diagnosis of SORO‐ESRD ‐ 4 males, 9 females, 12 Caucasians/one other, age 45 (18–83) years. Serum creatinine was 1.4 (0.8–1.7) mg/dL in the last year before hemodialysis initiation. Initial hemodialysis access was a dialysis catheter in all 13 patients. AKI precipitating SORO‐ESRD followed acute rejection (4), postoperative (2), tubulo‐interstitial nephritis (2), unknown (2), infection/sepsis (1), contrast nephropathy (1), BKV nephropathy (1), and cardio‐renal syndrome (1). Renal allograft survival was 1469 (277–4939) days (4 years). Renal allograft biopsies were available in 9/14 (69%) RTRs ‐ Four showed acute rejection, two of which followed interruption of immunosuppression, three revealed acute tubular necrosis and four others also showed chronic transplant glomerulopathy. Time on hemodialysis was 856 (129–1630) days (2.4 years). 5/13 RTRs with SORO‐ESRD (38%) died ‐ 3 (60%) following cardiac arrest, 2 (40%) after stopping hemodialysis. 4/13 (31%) were re‐transplanted in the period of this study.Conclusion: SORO‐ESRD contributed significantly to late renal allograft loss and return to hemodialysis with 100% initial dialysis catheter rate. Potentially preventable causes of AKI leading to SORO‐ESRD were identified. The application of experience gained from such studies would help reduce late renal allograft loss and the need for re‐transplantation. This would further help reduce the yawning gap between need and availability of donor kidney organs both here in the United States and around the world. Larger studies are warranted.

There is mounting evidence that forward heart failure as manifested by low cardiac output alone does not define the degree of renal dysfunction in cardiorenal syndrome. As a result, the term “congestive renal failure” was coined in 2012 by Ross to depict the role of renal venous hypertension in type 1 acute cardiorenal syndrome. If so, aggressive decongestive therapies, either through mechanical ultrafiltration with dialysis machines or pharmacologic ultrafiltration with potent diuretics, would lead to improved cardio and renal outcomes. Nevertheless, as recently as 2012, a review of this literature had concluded that a renal venous hypertension-directed approach using diuretics to manage cardio-renal syndrome was yet to be fully investigated. We, in this review, with three consecutive case series, describe our experience with pharmacologic decongestive diuresis in this paradigm of care and argue for studies of such therapeutic interventions in the management of cardiorenal syndrome. Finally, based on our observations in the Renal Unit, Mayo Clinic Health System, in Northwestern Wisconsin, we have hypothesized that patients with cardiorenal syndrome presenting with accelerated rising Pro B Naturetic Peptide levels appear to represent a group that would have good cardio- and renal-outcomes with such decongestive pharmacologic therapies.

Creatinine is produced in muscle metabolism as the end-product of creatine phosphate and is subsequently excreted principally by way of the kidneys, predominantly by glomerular filtration. Blood creatinine assays constitute the most common clinically relevant measure of renal function. The use of individual patient-level real-time serum creatinine trajectories provides a very attractive and tantalizing methodology in nephrology practice. Topics covered in this review include acute kidney injury (AKI) with its multifarious rainbow spectrum of renal outcomes; the stimulating vicissitudes of the diverse patterns of chronic kidney disease (CKD) to end-stage renal disease (ESRD) progression, including the syndrome of rapid onset end stage renal disease (SORO-ESRD); the syndrome of late onset renal failure from angiotensin blockade (LORFFAB); and post-operative AKI linked with the role of intra-operative hypotension in patients with diabetes mellitus and suspected diabetic nephropathy with CKD. We conclude that the study of individual patient-level serum creatinine trajectories, albeit a neglected and forgotten diagnostic methodology for diabetic CKD prognostication and prediction, is a most useful diagnostic tool, both in the short-term and in the long-term practice of nephrology. The analysis of serum creatinine trajectories, both in real time and retrospectively, indeed provides supplementary superior diagnostic and prognostic insights in the management of the nephrology patient.