Rhabdomyolysis in an HIV cohort: epidemiology, causes and outcomes.

BackgroundThe Literature on rhabdomyolysis in the HIV-positive population is sparse and limited. We aimed to explore the incidence, patient characteristics, etiologies and outcomes of rhabdomyolysis in a cohort of HIV-positive patients identified through the Johns Hopkins HIV clinical registry between June 1992 and April 2014.MethodsA retrospective analysis of 362 HIV-positive patients with non-cardiac CK elevation ≥1000 IU/L was performed. Both inpatients and outpatients were included. Incidence rate and potential etiologies for rhabdomyolysis were ascertained. The development of acute kidney injury (AKI, defined as doubling of serum creatinine), need for dialysis, and death in the setting of rhabdomyolysis were determined. Logistic regression was used to evaluate the association of peak CK level with the development of AKI.ResultsThree hundred sixty two cases of rhabdomyolysis were identified in a cohort of 7079 patients with a 38,382 person years follow-up time. The incidence rate was nine cases per 1000 person-years (95% CI: 8.5-10.5). Infection was the most common etiology followed by compression injury and drug/alcohol use. One-third of cases had multiple potential etiologies. AKI developed in 46% of cases; 20% of which required dialysis. Thirteen percent died during follow-up. After adjustment, AKI was associated with higher CK (OR 2.05 for each 1-log increase in CK [95% CI: 1.40-2.99]), infection (OR 5.48 [95% CI 2.65-11.31]) and higher HIV viral load (OR 1.22 per 1-log increase [95% CI: 1.03-1.45]).ConclusionRhabdomyolysis in the HIV-positive population has many possible causes and is frequently multifactorial. HIV-positive individuals with rhabdomyolysis have a high risk of AKI and mortality

Peri-renal adipose inflammation contributes to renal dysfunction in a non-obese prediabetic rat model: Role of anti-diabetic drugs

Diabetic nephropathy is a major health challenge with considerable economic burden and significant impact on patients’ quality of life. Despite recent advances in diabetic patient care, current clinical practice guidelines fall short of halting the progression of diabetic nephropathy to end-stage renal disease. Moreover, prior literature reported manifestations of renal dysfunction in early stages of metabolic impairment prior to the development of hyperglycemia indicating the involvement of alternative pathological mechanisms apart from those typically triggered by high blood glucose. Here, we extend our prior research work implicating localized inflammation in specific adipose depots in initiating cardiovascular dysfunction in early stages of metabolic impairment. Non-obese prediabetic rats showed elevated glomerular filtration rates and mild proteinuria in absence of hyperglycemia, hypertension, and signs of systemic inflammation. Isolated perfused kidneys from these rats showed impaired renovascular endothelial feedback in response to vasopressors and increased flow. While endothelium dependent dilation remained functional, renovascular relaxation in prediabetic rats was not mediated by nitric oxide and prostaglandins as in control tissues, but rather an upregulation of the function of epoxy eicosatrienoic acids was observed. This was coupled with signs of peri-renal adipose tissue (PRAT) inflammation and renal structural damage. A two-week treatment with non-hypoglycemic doses of metformin or pioglitazone, shown previously to ameliorate adipose inflammation, not only reversed PRAT inflammation in prediabetic rats, but also reversed the observed functional, renovascular, and structural renal abnormalities. The present results suggest that peri-renal adipose inflammation triggers renal dysfunction early in the course of metabolic disease.This study was supported by American University of Beirut Faculty of Medicine Medical Practice Plan grant #320148 granted to AFE. The funding body had no role in the design of the study or collection, analysis, and interpretation of data or in writing the manuscript

Conservative kidney management and kidney supportive care:core components of integrated care for people with kidney failure

Integrated kidney care requires synergistic linkage between preventative care for people at risk for chronic kidney disease and health services providing care for people with kidney disease, ensuring holistic and coordinated care as people transition between acute and chronic kidney disease and the 3 modalities of kidney failure management: conservative kidney management, transplantation, and dialysis. People with kidney failure have many supportive care needs throughout their illness, regardless of treatment modality. Kidney supportive care is therefore a vital part of this integrated framework, but is nonexistent, poorly developed, and/or poorly integrated with kidney care in many settings, especially in low- and middle-income countries. To address this, the International Society of Nephrology has (i) coordinated the development of consensus definitions of conservative kidney management and kidney supportive care to promote international understanding and awareness of these active treatments; and (ii) identified key considerations for the development and expansion of conservative kidney management and kidney supportive care programs, especially in low resource settings, where access to kidney replacement therapy is restricted or not available. This article presents the definitions for conservative kidney management and kidney supportive care; describes their core components with some illustrative examples to highlight key points; and describes some of the additional considerations for delivering conservative kidney management and kidney supportive care in low resource settings.</p

Hungry bone syndrome two weeks after starting cinacalcet: a call for caution.

Cinacalcet is an effective and safe alternative to parathyroidectomy in end stage renal disease (ESRD) patients with secondary hyperparathyroidism. Hypocalcemia is a known complication of treatment that is usually readily reversible upon discontinuation of the drug. It rarely manifests severely and symptomatically requiring hospital admission. We present the case of a 55 year old man with severe, symptomatic and prolonged hypocalcemia that occurred 2 weeks after starting cinacalcet. Cinacalcet induced a state of pharmacological parathyroidectomy with subsequent hungry bone syndrome. Serum calcium returned to normal range after 4 weeks of stopping the drug while receiving high doses of elemental calcium and vitamin D receptor activation therapy (VDRA)

Corrigendum to “Peri-renal adipose inflammation contributes to renal dysfunction in a non-obese prediabetic rat model: Role of anti-diabetic drugs” [Biochem. Pharmacol. 186 (2021) 114491] (Biochemical Pharmacology (2021) 186, (S0006295221000873), (10.1016/j.bcp.2021.114491))

We regret to report that a mistake occurred in preparation of Fig. 4. The modified figure is included below. We apologize for any confusion this might have created

Reduction of intracerebral hemorrhage in hemodialysis patients after reducing aspirin use: A quality-assurance observational study

<div><p>There is so far no international consensus concerning the prescription of antithrombotic agents in hemodialysis patients. It is not clear yet why they cause more bleeding in some patients and are beneficial in others. We therefore tried to find out what triggers bleeding in this population. This is an observational before-and-after study that included all patients undergoing hemodialysis in our center between 2005 and 2015. We divided the study into two phases: phase one (125 patients) where aspirin was used without restrictions and phase two (110 patients) where aspirin was avoided in severe hypertension and primary prevention. We aimed to assess the differential occurrence of intracerebral hemorrhage between the two phases and the cardiovascular mortality of patients whether on aspirin or not. Bleeding events occurred in 12.8% of patients in phase one and 13.6% in phase two (<i>p</i> = 0.85). Seven out of 125 patients (6%) in phase one experienced intracerebral hemorrhage and none in phase two. Intracerebral hemorrhage was significantly increased in those with the combination of aspirin and severe hypertension (<i>p</i> = 0.003). Aspirin and acenocoumadin were significantly associated with total bleeding (OR = 3.81 and 4.85 with <i>p</i> = 0.005 and 0.001 respectively). Cardiovascular mortality did not differ between phase one and two whether patients were on aspirin or not (<i>p</i> = 0.45 and 0.31 respectively). Minimizing aspirin use in hemodialysis patients with severe hypertension reduced intracerebral bleeding without a significant difference in cardiovascular mortality.</p></div

Demographic and baseline clinical characteristics of patients in the two phases.

<p>Demographic and baseline clinical characteristics of patients in the two phases.</p

Outcomes: Bleeding and death in the two phases.

<p>Outcomes: Bleeding and death in the two phases.</p

Antithrombotic agents distribution in the two phases, n (%).

<p>Antithrombotic agents distribution in the two phases, n (%).</p