Clinical outcomes with a systolic blood pressure lower than 120 mmHg in older patients with high disease burden.

BACKGROUND: The target blood pressure in older patients is controversial. Recent studies provided clinical evidence supporting a target systolic blood pressure <120 mmHg in patients >50 years at high risk of cardiovascular events. METHODS: Retrospective study of 380 consecutive patients ≥60 years with stages 1-5 pre-dialysis chronic kidney disease seen between January 2013 and November 2015. The outcomes of a systolic blood pressure <120 mmHg in older patients with chronic kidney disease and multiple comorbidities were analyzed. RESULTS: Sixty-eight patients had a systolic blood pressure <120 mmHg, 312 patients had a systolic blood pressure ≥120 mmHg. Forty-three patients died during the follow up (11.3%). Patients with a systolic blood pressure <120 mmHg had a higher risk of death: 21 (30.9%) vs 22 (7%). Primary cause of death: Cardiovascular: 11 (25.6%), infectious 9 (20.9%), cancer 5 (11.6%), renal failure 6 (13.9%), COPD/pulmonary fibrosis 2 (4.6%), end stage liver disease 3 (6.9%), traumatic brain injury 1 (2.3%), gastrointestinal hemorrhage 4 (9.3%), complications of diabetes 1 (2.3%), unknown 1 (2.3%). After adjusting for confounding factors, a systolic blood pressure <120 mmHg remained associated with increased mortality. There was a trend to more cardiovascular outcomes in those with a lower blood pressure. CONCLUSIONS: A systolic blood pressure below 120 mmHg in older patients with high disease burden was associated with adverse outcomes. Individualization of blood pressure therapy to each specific patient is warranted.

Avoidance of polypharmacy and excessive blood pressure control is associated with improved renal function in older patients.

BACKGROUND: Elderly patients are particularly susceptible to polypharmacy. The present study evaluated the renal effects of optimizing potentially nephrotoxic medications in an older population. METHODS: Retrospective study of patients' ≥ 60 years treated between January of 2013 and February of 2015 in a Nephrology Clinic. The renal effect of avoiding polypharmacy was studied. RESULTS: Sixty-one patients were studied. Median age was 81 years (range 60-94). Twenty-five patients (41%) were male. NSAIDs alone were stopped in seven patients (11.4%), a dose reduction in antihypertensives was done in 11 patients (18%), one or more antihypertensives were discontinued in 20 patients (32.7%) and discontinuation and dose reduction of multiple medications was carried out in 23 patients (37.7%). The number of antihypertensives was reduced from a median of 3 (range of 0-8) at baseline to a median of 2 (range 0-7), p < 0.001 after intervention. After intervention, the glomerular filtration rate (GFR) improved significantly, from a baseline of 32 ± 15.5 cc/min/1.73 m(2) to 39.5 ± 17 cc/min/1.73 m(2) at t1 (p < 0.001) and 44.5 ± 18.7 cc/min/1.73 m(2) at t2 (p < 0.001 vs. baseline). In a multivariate model, after adjusting for ACEIs/ARBs discontinuation/dose reduction, NSAIDs use and change in DBP, an increase in SBP at time 1 remained significantly associated with increments in GFR on follow-up (estimate = 0.20, p = 0.01). CONCLUSIONS: Avoidance of polypharmacy was associated with an improvement in renal function.

Evaluation of "Loss" and "End stage renal disease" after acute kidney injury defined by the Risk, Injury, Failure, Loss and ESRD classification in critically ill patients.

PURPOSE: The Risk, Injury, Failure, Loss and ESRD (RIFLE) classification has been widely accepted for the definition of acute kidney injury (AKI); however, no study has described in detail the last two stages of the classification: "Loss" and "ESRD". We aim to describe and evaluate the development of "Loss" and "ESRD" in a group of critically ill patients. METHODS: We conducted a retrospective analysis of cases prospectively collected from the Acute Physiology and Chronic Health Assessment (APACHE III) database. Subjects were consecutive critically ill patients >18 years of age admitted to three ICUs of two tertiary care academic hospitals, from January 2003 through August 2006, excluding those who denied research authorization, chronic hemodialysis therapy, kidney transplant recipients, readmissions, and admissions for less than 12 h for low risk monitoring. RESULTS: 11,644 patients were included in the study. The median age was 66 (interquartile range, 52-76), 90% were Caucasians and 54% of the patients were male. Half of the patients developed AKI, and most of the patients were in the Risk and Injury stages. From the patients that developed AKI, a total of 1,065 (19%) patients required renal replacement therapy (RRT), 415 (39%) underwent continuous renal replacement therapy (CRRT) and 650 (61%) underwent intermittent hemodialysis. A total of 281 patients on RRT did not survive hospital discharge, 97 patients progressed to "Loss", and 282 patients progressed to "ESRD". After multivariable adjustment, the progression to "ESRD" was associated with higher baseline creatinine, odds ratio (OR) 1.19 per every increase in creatinine of 0.1 mg/dl (95% CI, 1.11-1.29) P < 0.001; and less frequent use of CRRT, OR 0.18 (95% CI, 0.11-0.29) P < 0.001. CONCLUSION: In this large retrospective study we found that almost 50% developed some form of AKI as defined by the RIFLE classification. Of these, 19% required RRT, and 4.9% progressed to "ESRD". "ESRD" was more likely in patients with elevated baseline creatinine and those treated with intermittent hemodialysis.

Prognostic value of dobutamine stress echocardiography in patients with chronic kidney disease.

BACKGROUND: Although dobutamine stress echocardiography (DSE) is cited in clinical guidelines for the evaluation of patients with chronic kidney disease (CKD), there are limited data regarding its prognostic utility in this setting. The current study assesses the prognostic value of DSE in patients with CKD. METHODS: Four hundred eighty-five patients with CKD (on renal dialysis or with creatinine > 3 mg/mL) who had DSE were followed for 2.3 +/- 1.8 years. RESULTS: One hundred eighty-eight (39%) patients died during follow-up. Patients with extensive ischemia (affecting > 25% of myocardial segments) had a 1- and 3-year survival rate of 77% and 48%, respectively, compared with 83% and 52% in those with lesser degrees (< or = 25% segments affected) of ischemia and with 88% and 70% in those with a normal DSE. In multivariate analyses, the percentage of ischemic segments on DSE was an independent predictor of all-cause mortality (hazard ratio, 1.40 per 25% increase; 95% CI, 1.16-1.68; P = .001). Inclusion of DSE data improved the predictive value of the best clinical model (chi2, 83.6-97.4; P = .003). CONCLUSION: In patients with CKD, the percentage of ischemic segments during DSE is an independent predictor of mortality and provides prognostic information that is incremental to clinical data.

A proliferative glomerulonephritis secondary to a monoclonal IgA.

A distinct entity mimicking immune-complex-mediated glomerulonephritis characterized by a proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits recently was described. We now report a case of a 35-year-old woman who presented with sudden onset of edema, proteinuria, hematuria, and hypertension. Renal biopsy showed diffuse endocapillary proliferation, mesangial cellularity, and amorphous material in the mesangium. Immunofluorescence examination showed mesangial and capillary wall staining for IgA (2+), C3 (2+), fibrinogen (2+), and lambda (2+). Congo red stain was negative. Electron microscopy showed mesangial and subendothelial deposits with a paracrystalline lattice-like substructure forming parallel linear arrays. Extensive laboratory evaluation showed a small population of monoclonal plasma cells with lambda restriction. The present case suggests that monoclonal IgA deposits also can cause proliferative glomerulonephritis. However, the presence of paracrystalline deposits in association with monoclonal IgA deposits has not been described previously.

Living donor kidney and autologous stem cell transplantation for primary systemic amyloidosis (AL) with predominant renal involvement.

Primary systemic amyloidosis (AL) is characterized by multiorgan deposition of monoclonal immunoglobulin light chain. Renal involvement is common and impaired kidney function is associated with reduced median survival. Autologous stem cell transplantation (SCT) for AL achieves superior response rates compared to chemotherapy alone but patients with end-stage renal disease (ESRD) may be excluded from consideration. A treatment approach consisting of living donor kidney transplantation (LDKTx) followed by autologous SCT was developed for AL with ESRD. Eight patients underwent LDKTx with immediate graft function. Two suffered unanticipated complications post-KTx and died 10 and 3 months later. Two cases of subclinical acute cellular rejection (ACR) and one case of clinical ACR occurred--all reversible with corticosteroid. Six patients had successful stem cell harvests performed and five of these underwent SCT with satisfactory trilineage engraftment. Renal function remained stable following SCT in four and was reduced in one due to infectious and bleeding complications. One patient, who has thus far elected not to undergo SCT, has proteinuria and histologic evidence of recurrent renal amyloidosis. This experience supports the feasibility of sequential living donor KTx and autologous SCT for carefully selected patients with ESRD due to AL.

Iodine toxicity treated with hemodialysis and continuous venovenous hemodiafiltration.

Continuous mediastinal irrigation with povidone-iodine is used commonly for treating severe postoperative mediastinitis. However, concurrent iodine toxicity has been reported, particularly in patients with renal dysfunction (likely because absorbed iodine is renally excreted). The authors were consulted on a 45-year-old patient with mediastinitis who had renal and hepatic dysfunction while being treated with mediastinal irrigation of povidone-iodine. The povidone-iodine irrigation was discontinued because he had toxic plasma iodine levels. Despite this, his condition worsened, and the iodine levels remained elevated. Thus, hemodialysis (HD) was initiated using high-flux membranes followed by continuous venovenous hemodiafiltration (CVVHDF; 2 L/h of hemofiltration and 2 L/h of HD). Plasma and effluent iodine levels were measured repeatedly to determine iodine clearance by these 2 modalities (HD, 120 mL/min; CVVHDF, 37 mL and 44 mL/min on days 1 and 2, respectively). Hepatic and renal functions improved with decreasing plasma iodine levels. Based on this experience and after reviewing the literature the authors conclude that: (1) iodine irrigation can increase blood iodine levels significantly, especially in the setting of renal failure, and lead to increased morbidity and mortality; (2) plasma iodine levels should be monitored in patients with renal insufficiency; and (3) HD and CVVHDF are effective at clearing iodine. The authors suggest that patients that are at high risk or already developing signs of iodine toxicity should have the iodine irrigation discontinued and may benefit from renal replacement therapy (RRT). Alternatively, concomitant RRT during iodine irrigation may be attempted to maintain the systemic iodine levels at nontoxic levels.