Syndrome of rapid onset ESRD accounted for high hemodialysis catheter use--results of a 13-year Mayo Clinic incident hemodialysis study.

BACKGROUND: The syndrome of rapid onset end-stage renal disease (SORO-ESRD) was first described in the journal Renal Failure in 2010. This is an acute precipitate unpredictable yet irreversible ESRD following acute kidney injury (AKI), as distinct from "classic" ESRD where chronic kidney disease (CKD)-ESRD progression was linear, time-dependent, and predictable. The overall impact of SORO-ESRD on ESRD outcomes in the adult US ESRD population remains speculative and called for larger studies. METHODS: A retrospective investigation of an incident adult ESRD population, Mayo Clinic, Rochester, 2001-2013. RESULTS: One hundred and forty-nine of 1461 (10%) incident patients with ESRD had SORO-ESRD - M:F = 76:73, age 62 (19-95) years, 139 (93%) native kidneys, and 10 (7%) renal transplant recipients (RTRs). The modal age group was 71-80 years. A total of 147 (99%) SORO-ESRD patients started first hemodialysis treatment via a dialysis catheter. Kidney biopsy in 10 RTRs and 34 native kidneys revealed acute tubular necrosis (ATN) as the commonest pathology. Cardiac arrest remained the leading cause of death among SORO-ESRD patients. CONCLUSIONS: SORO-ESRD accounted for 149 (10%) of 1461 incident ESRD patients. There was no gender disparity. The older population was more susceptible. Ninety-nine percent (99%) of SORO-ESRD patients started their first hemodialysis treatment via a dialysis catheter, a major negative impact on AV fistula first programs. ATN was the leading pathologic diagnosis. We conclude that SORO-ESRD contributes significantly to incident ESRD here in the USA including renal allograft loss. Efforts to reduce AKI incidence or renoprevention demand more attention and priority.

Pseudo-arterial Temporary Hemodialysis Catheter Placement in the Left Internal Jugular Vein Ipsilateral to a Preexisting Brachio-axillary Arteriovenous Graft.

Internal jugular vein (IJV) cannulation was originally described by English et al. in 1969 as the safest approach. Carotid artery puncture had an incidence rate of 4-6% before ultrasound guidance. We encountered an unexpected sequence of events following the ultrasound-guided placement of a temporary HD catheter in the left IJV. The postprocedure chest radiograph was misinterpreted as an arterial misplacement, the blood return was correspondingly bright red, and simultaneous blood gas analyses from the left IJV catheter and a right radial artery were near mirror images. Subsequently, a transducer to the catheter showed a clearly venous waveform with a pressure of 40 mmHg. Thus, it was realized that the cacophony of missteps, misjudgments, and misinterpretations was due to the contiguous presence of a functional left brachio-axillary arteriovenous (AV) graft. To our knowledge, this is the first such report of this phenomenon of a pseudo-arterial central venous catheter placement in the IJV.

A Novel Diagnostic Approach for Suspected Icodextrin Pleural Effusion in a Peritoneal Dialysis Patient.

Symptomatic pleural effusion secondary to pleuroperitoneal communication in patients undergoing peritoneal dialysis (PD) occurs in approximately 2% of patients undergoing continuous ambulatory PD. The classic presentation is that of a low-protein, high-glucose pleural aspirate consistent with the high dextrose concentrations present in standard PD fluids, hence the name sweet hydrothorax. Nevertheless, the increasing use of icodextrin calls for an innovative bedside diagnostic approach because icodextrin does not contain high concentrations of dextrose after all. We describe a patient with newly symptomatic right pleural effusion 2 months after starting continuous ambulatory PD with 2 exchanges every 12 hours. Prompt relief was achieved with therapeutic thoracentesis, but the pleural aspirate had less than 2 g/dL of protein (to convert to g/L, multiply by 10) and a glucose level of 108 mg/dL (to convert to mmol/L, multiply by 0.0555), lower than the blood glucose level of 139 mg/dL in the emergency department earlier the same night. The patient was allergic to iodinated contrast. We, therefore, used an innovative approach with biochemical fingerprint analysis of simultaneous pleural and peritoneal fluids for electrolytes, urea, creatinine, and measured osmolality. With the increasing use of icodextrin in contemporary PD worldwide, this innovative tactic is cheap, is easily available, and does not require sophisticated, expensive, and often unavailable options, such as isotope studies, dye studies, and iodinated contrast-enhanced computed tomography. To our knowledge, this is the first time that biochemical fingerprint analysis of simultaneous pleural and peritoneal fluids has been reported in the literature.

Severe symptomatic acute hyponatremia in traumatic brain injury responded very rapidly to a single 15 mg dose of oral tolvaptan; a Mayo Clinic Health System hospital experience - need for caution with tolvaptan in younger patients with preserved renal function.

Tolvaptan is now well established as a potent pharmaceutical agent for symptomatic hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (SIADH), congestive heart failure and liver cirrhosis. Previous studies had recruited older (63-65 years) patients with mild renal impairment (serum creatinine, 1.3-1.4 mg/dl). A 2012 report in the Journal of Neurology, Neurosurgery & Psychiatry described tolvaptan as a "lifesaving drug". A major outcome concern in the treatment of chronic hyponatremia is potentially fatal pontine demyelination from over-rapid correction of serum sodium >0.5 mEq/dL/h. The maximum reported correction of serum sodium within 24 hours was 13 mEq/L in a case of SIADH. We recently experienced the dramatic correction of hyponatremia at 1 mEq/dL/h over 18 hours, following 15 mg of oral tolvaptan in a 32-year old male patient with normal kidney function (serum creatinine 0.76 mg/dL), following traumatic brain injury (TBI). Tolvaptan is indeed an effective and life-saving drug for post-TBI hyponatremia. However, we strongly recommend the use of lower doses of tolvaptan (≤15 mg/d) in younger patients with more preserved renal function to avoid the development of life-threatening pontine demyelination.

A Mayo Clinic 13-year investigation of the syndrome of rapid onset ESRD among renal transplant recipients: An analysis of the implications of renal allograft biopsy results.

INTRODUCTION: 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.

The Ignored Role of Intraoperative Hypotension in Producing Postoperative Acute Kidney Injury-An Obligatory Appeal for More Preventative Nephrology.

BACKGROUND/OBJECTIVE: Intraoperative hypotension (IOH) invariably follows the induction of general anesthesia during surgical operations. The current prevailing and predominant consensus is that IOH has immense clinical benefits such as reduced bleeding, less need for blood transfusions, and shorter surgery times. Simultaneously, it is assumed that IOH is devoid of adverse renal, hepatic and neurological consequences. Emerging new evidence and our experiences suggest a strong link between IOH and postoperative acute kidney injury (AKI). Method/Case Reports: We report on three case presentations to illustrate the impact of IOH on postoperative AKI. CONCLUSION: Our recent experiences suggest and show a link between IOH and postoperative AKI. Sun et al. (2015) recently demonstrated that postoperative AKI was associated with sustained intraoperative hypotensive periods of MAP <55 and <60 mm Hg, respectively, in a graded pattern. Our experiences and new emerging Surgery-AKI literature provide an impetus for clinical trials to be set up and completed to determine whether interventions that promptly treat IOH, or better still that prevent IOH, and that are tailored to suit individual patient physiology, would reduce the risk of AKI. We posit that IOH is a neglected cause of postoperative AKI. We call for a preventative nephrology paradigm shift and the targeting of MAP ≥ 60 mm Hg and/or SBP ≥ 90 mm Hg during surgical procedures. Particularly in sub-Saharan Africa with its paucity of renal replacement therapy options to manage kidney failure, every effort to limit AKI, SORO-ESRD and exacerbation of kidney dysfunction in general, must be vigorously applied.

Acute Kidney Injury in Heart Failure Revisited-The Ameliorating Impact of "Decongestive Diuresis" on Renal Dysfunction in Type 1 Acute Cardiorenal Syndrome: Accelerated Rising Pro B Naturetic Peptide Is a Predictor of Good Renal Prognosis.

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.

A curious case of persistently relapsing hyperkalemia in an ESRD patient on maintenance hemodialysis following bioprosthetic aortic valve replacement - a potential case for the use of the new agent, patiromer, for hyperkalemia management.

Hyperkalemia is not uncommon in patients with end-stage renal disease (ESRD) on maintenance hemodialysis, often related to dietary indiscretion, following the prolonged inter-dialytic weekend interval in patients on thrice weekly hemodialysis treatments, and sometimes the adverse effects of medications such as RAAS blocking agents. Moreover, hyperkalemia following extended cardiac surgery can result from the use of high-potassium containing cardioplegic solutions used during cardiopulmonary bypass. Nevertheless, different from the foregoing, in the nephrology literature, there have been very rare reports of potentially life-threatening hyperkalemia following cardiac valve replacement procedure. We recently encountered an unusual case of persistent relapsing hyperkalemia complicating aortic valve replacement (AVR) in a 53-year-old obese Caucasian male patient despite repeated daily intermittent hemodialysis treatments. Our case report is the first to clearly demonstrate the yo-yo recurrence of newly observed episodes of hyperkalemia reappearing despite repeated treatments.

Pleuritic chest pain from portal hypertensive gastropathy in ESRD patient with autosomal dominant polycystic kidney disease misdiagnosed as pericarditis.

Portal hypertensive gastropathy (PHG) is a gastric mucosal lesion complicating portal hypertension, with higher prevalence in decompensated cirrhosis. PHG can sometimes complicate autosomal dominant polycystic kidney disease (ADPKD) due to the presence of multiple liver cysts. Besides, PHG is known to present as chest pain, with or without hematemesis. Other causes of chest pain in ADPKD include referred chest pain from progressively enlarging kidney cysts, and rare pericardial cysts. Chest pain, especially if pleuritic, in end-stage renal disease (ESRD) patients, is often ascribed to uremic pericarditis. We present recurrent pleuritic chest pain in a 24-year old ESRD patient with ADPKD that was initially misdiagnosed as uremic pericarditis. It was ultimately shown to represent symptomatic PHG with excellent therapeutic response to proton pump inhibitors.

Intraoperative hypotension - a neglected causative factor in hospital-acquired acute kidney injury; a Mayo Clinic Health System experience revisited.

Acute kidney injury (AKI) is a relatively common complication of cardiothoracic surgery and has both short- and long-term survival implications, even when AKI does not progress to severe renal failure. Given that currently, there are no active effective treatments for AKI, other than renal replacement therapy when indicated, the focus of clinicians ought to be on prevention and risk factor management. In the AKI-surgery literature, there exists this general consensus that intraoperative hypotension (IH) following hypotensive anesthesia (HA) or controlled hypotension (CH) in the operating room has no significant short-term and long-term impacts on renal function. In this review, we examine the basis for this consensus, exposing some of the flaws of the clinical study data upon which this prevailing consensus is based. We then describe our experiences in the last decade at the Mayo Clinic Health System, Eau Claire, in Northwestern Wisconsin, USA, with two selected case presentations to highlight the contribution of IH as a potent yet preventable cause of post-operative AKI. We further highlight the causative although neglected role of IH in precipitating postoperative AKI in chronic kidney disease (CKD) patients. We show additional risk factors associated with this syndrome and further make a strong case for the elimination of IH as an achievable mechanism to reduce overall, the incidence of hospital acquired AKI. We finally posit that as the old saying goes, prevention is indeed better than cure.

Diabetic Nephropathy and CKD-Analysis of Individual Patient Serum Creatinine Trajectories: A Forgotten Diagnostic Methodology for Diabetic CKD Prognostication and Prediction.

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.

Chronic kidney disease prediction is an inexact science: The concept of "progressors" and "nonprogressors".

In 2002, the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) instituted new guidelines that established a novel chronic kidney disease (CKD) staging paradigm. This set of guidelines, since updated, is now very widely accepted around the world. Nevertheless, the authoritative United States Preventative Task Force had in August 2012 acknowledged that we know surprisingly little about whether screening adults with no signs or symptoms of CKD improve health outcomes and that we deserve better information on CKD. More recently, the American Society of Nephrology and the American College of Physicians, two very well respected United States professional physician organizations were strongly at odds coming out with exactly opposite recommendations regarding the need or otherwise for "CKD screening" among the asymptomatic population. In this review, we revisit the various angles and perspectives of these conflicting arguments, raise unanswered questions regarding the validity and veracity of the NKF KDOQI CKD staging model, and raise even more questions about the soundness of its evidence-base. We show clinical evidence, from a Mayo Clinic Health System Renal Unit in Northwestern Wisconsin, United States, of the pitfalls of the current CKD staging model, show the inexactitude and unpredictable vagaries of current CKD prediction models and call for a more cautious and guarded application of CKD staging paradigms in clinical practice. The impacts of acute kidney injury on CKD initiation and CKD propagation and progression, the effects of such phenomenon as the syndrome of late onset renal failure from angiotensin blockade and the syndrome of rapid onset end stage renal disease on CKD initiation, CKD propagation and CKD progression to end stage renal disease all demand further study and analysis. Yet more research on CKD staging, CKD prognostication and CKD predictions is warranted. Finally and most importantly, cognizant of the very serious limitations and drawbacks of the NKF K/DOQI CKD staging model, the need to individualize CKD care, both in terms of patient care and prognostication, cannot be overemphasized.