In various human diseases, an increase in capillary permeability to proteins leads to the loss of protein-rich fluid from the intravascular to the interstitial space. Although sepsis is the disease ...most commonly associated with this phenomenon, many other diseases can lead to a “sepsis-like” syndrome with manifestations of diffuse pitting edema, exudative serous cavity effusions, noncardiogenic pulmonary edema, hypotension, and, in some cases, hypovolemic shock with multiple-organ failure. The term capillary leak syndrome has been used to describe this constellation of disease manifestations associated with an increased capillary permeability to proteins. Diseases other than sepsis that can result in capillary leak syndrome include the idiopathic systemic capillary leak syndrome or Clarkson’s disease, engraftment syndrome, differentiation syndrome, the ovarian hyperstimulation syndrome, hemophagocytic lymphohistiocytosis, viral hemorrhagic fevers, autoimmune diseases, snakebite envenomation, and ricin poisoning. Drugs including some interleukins, some monoclonal antibodies, and gemcitabine can also cause capillary leak syndrome. Acute kidney injury is commonly seen in all of these diseases. In addition to hypotension, cytokines are likely to be important in the pathophysiology of acute kidney injury in capillary leak syndrome. Fluid management is a critical part of the treatment of capillary leak syndrome; hypovolemia and hypotension can cause organ injury, whereas capillary leakage of administered fluid can worsen organ edema leading to progressive organ injury. The purpose of this article is to discuss the diseases other than sepsis that produce capillary leak and review their collective pathophysiology and treatment.
Cardio-renal syndrome is a commonly encountered problem in clinical practice. Its pathogenesis is not fully understood. The purpose of this article is to highlight the interaction between the ...cardiovascular system and the renal system and how their interaction results in the complex syndrome of cardio-renal dysfunction. Additionally, we outline the available therapeutic strategies to manage this complex syndrome.
The most common bariatric surgery is Roux-en-Y gastric bypass (RYGB), which has been associated with hyperoxaluria and nephrolithiasis. We report a novel association of RYGB with renal insufficiency ...as a result of oxalate nephropathy.
Eleven cases of oxalate nephropathy after RYGB were identified from the Renal Pathology Laboratory of Columbia University. The clinical features, pathologic findings, and outcomes are described.
Patients were predominantly white (72.7%) with a mean age of 61.3 yr. Indications for RYGB included morbid obesity (eight patients) and reconstruction after total gastrectomy for gastric cancer (three patients). All 11 patients had a history of hypertension, and 9 were diabetic. Patients presented with acute renal failure, often superimposed on mild chronic renal insufficiency (n = 7), at a median of 12 mo after RYGB. The mean creatinine at baseline, at discovery of acute renal failure, and at biopsy was 1.5, 5.0, and 6.5 mg/dl, respectively. Renal biopsies revealed diffuse tubular degenerative changes, abundant tubular calcium oxalate deposits, and varying degrees of tubulointerstitial scarring. In addition, seven biopsies had underlying diabetic glomerulosclerosis and two had glomerulosclerosis attributable to obesity and hypertension. Eight of 11 patients rapidly progressed to ESRD and required hemodialysis at a mean of 3.2 wk after renal biopsy. The remaining three patients were left with significant chronic kidney disease.
Oxalate nephropathy is an underrecognized complication of RYGB and typically results in rapid progression to ESRD. Patients with pre-existing renal disease may be at higher risk for this complication.
Contrast-associated acute kidney injury (CA-AKI), a potential complication of cardiovascular interventions that require radiocontrast administration, is associated with increased morbidity, ...mortality, and length of hospital admission. CA-AKI is particularly prevalent among patients with chronic kidney disease and comorbidities such as advanced age and diabetes. This review briefly discusses the evidence-based strategies to minimize CA-AKI. In addition, technical details of procedures to minimize the contrast volume, i.e., ultra-low contrast angiography and zero contrast percutaneous intervention, along with several illustrative cases are presented.
Coronary artery disease is highly prevalent in chronic kidney disease (CKD) and is a risk factor for contrast-associated acute kidney injury (CA-AKI), a complication of cardiovascular procedures that require contrast administration (e.g., coronary angiography, percutaneous coronary intervention PCI). CA-AKI has a major impact on morbidity, mortality, and healthcare resource utilization. The incidence of CA-AKI is particularly high in patients with pre-existing CKD, advanced age and comorbidities that increase the likelihood of CKD. The focus of the present review is to provide a brief overview on the assessment of the risk for and prevention of CA-AKI in patients undergoing angiography and PCI, including recognition of the important patient- and procedure-related factors that may contribute to CA-AKI. Preventive and treatment strategies, the mainstay of which is volume repletion by normal saline, are briefly discussed. The main focus of the review is placed on technical details of contrast minimization techniques, including ultra-low contrast angiography and zero-contrast PCI. Operator competence in such techniques is important to ensure that procedural challenges in patients with CKD, like vessel calcification, multivessel disease and complex anatomical subsets, are effectively addressed by PCI while minimizing the risk of CA-AKI.
Systemic Lupus Erythematosis (SLE) is a heterogeneous and complex disease produced by diverse pathogenic events in the innate and adaptive immune system. Lupus nephritis affects over half of all ...patients with lupus and leads to substantial morbidity and mortality. This review presents our current understanding of the development of lupus nephritis and examines the role of genetics and epigenetics in further elucidating the pathogenesis of the disease. Advancements in genomics are leading the way to better understanding and novel biologic therapies for SLE.
Lupus Nephritis: Treatment of Resistant Disease Kalloo, Sean; Aggarwal, Nidhi; Mohan, Prince ...
Clinical journal of the American Society of Nephrology,
01/2013, Letnik:
8, Številka:
1
Journal Article
Recenzirano
Odprti dostop
Lupus nephritis (LN) remains a major cause of ESRD and is associated with a >4-fold increase in mortality and significant morbidity in patients with lupus. The treatment of LN has evolved ...significantly over the past decade due to data from well conducted randomized controlled trials. We are currently in an era in which effective regimens exist in the form of induction and maintenance agents. Histopathologic classification of LN remains one of the main factors guiding therapy.
Antineutrophil cytoplasmic autoantibody (ANCA)-associated pauci-immune glomerulonephritis (GN) is the most common finding in very elderly patients biopsied for acute kidney injury. Appropriate ...treatment strategies in this age group are currently undefined since it is unclear whether the benefits of immunosuppression exceed the risks. We retrospectively evaluated a cohort of 78 cases of biopsy-proven pauci-immune GN in individuals aged >80 years of whom 72% were p-ANCA and 20% were c-ANCA positive. The patients treated with immunosuppression had a significantly lower incidence of end-stage renal disease (ESRD) 1 year after biopsy (36%) compared with untreated patients (73%; P=0.03). Only peak serum creatinine before biopsy and the use of immunosuppression influenced progression to ESRD. There was no significant difference in the 1-year mortality rates between these groups (46 vs 64%; P=0.3). However, when follow-up was extended beyond 2 years, immunosuppression was associated with a lower risk of death (HR 0.33, 95% CI 0.11–0.97) and death or ESRD (HR 0.16, 95% CI 0.06–0.42) in multivariable models.
Abstract Objective Although the outcomes of patients with cardiogenic shock remain poor, short-term mechanical circulatory support has become an increasingly popular modality for hemodynamic ...assistance and organ preservation. Because the kidney is exquisitely sensitive to poor perfusion, acute kidney injury is a common sequela of cardiogenic shock. This study examines the incidence and clinical impact of acute kidney injury in patients with short-term mechanical circulatory support for cardiogenic shock. Methods Retrospective review was performed of 293 consecutive patients with cardiogenic shock who were treated with short-term mechanical circulatory support. The well-validated 2014 Kidney Disease Improving Global Outcomes criteria were used to stage acute kidney injury. Outcomes of interest were long-term mortality and renal recovery. Results Acute kidney injury developed in 177 of 293 patients (60.4%), of whom 113 (38.6%) were classified with stage 3 (severe). Kaplan–Meier survival estimates indicated a 1-year survival of 49.2% in the nonsevere (stages 0-2) acute kidney injury cohort versus 27.3% in the severe acute kidney injury cohort ( P < .001). Multivariable Cox regression demonstrated that severe acute kidney injury was a predictor of long-term mortality (hazard ratio, 1.54; confidence interval, 1.10-2.14; P = .011). Among hospital survivors, renal recovery occurred more frequently (82.4% vs 63.2%, P = .069) and more quickly (5.6 vs 24.5 days, P < .0001) in the nonsevere than in the severe acute kidney injury group. Conclusions Acute kidney injury is common and frequently severe in patients in cardiogenic shock treated with short-term mechanical circulatory support. Milder acute kidney injury resolves with survival comparable to patients without acute kidney injury. Severe acute kidney injury is an independent predictor of long-term mortality. Nonetheless, many surviving patients with acute kidney injury do experience gradual renal recovery.
This study sought to determine correlates and consequences of contrast-associated acute kidney injury (CA-AKI) on clinical outcomes in patients with or without pre-existing chronic kidney disease ...(CKD).
The incidence and impact of CA-AKI on clinical outcomes during contemporary percutaneous coronary intervention (PCI) are not fully defined.
The ADAPT-DES (Assessment of Dual AntiPlatelet Therapy With Drug Eluting Stents) study was a prospective, multicenter registry of 8,582 patients treated with ≥1 drug-eluting stent(s). CA-AKI was defined as a post-PCI increase in serum creatinine of >0.5 mg/dL or a relative increase of ≥25% compared with pre-PCI. CKD was defined as estimated glomerular filtration rate <60 mL/min/1.73 m2. The primary endpoint was the 2-year rate of net adverse clinical events (NACE): All-cause mortality, myocardial infarction (MI), definite or probable stent thrombosis, or major bleeding.
Of 7287 (85%) patients with evaluable data, 476 (6.5%) developed CA-AKI. In a multivariable model, older age, female sex, Caucasian race, congestive heart failure, diabetes, hypertension, CKD, presentation with ST-segment elevation MI, Killip class II to IV, radial access, intra-aortic balloon pump use, hypotension, and number of stents were independent predictors of CA-AKI. The 2-year NACE rate was higher in patients with CA-AKI (adjusted HR: 1.88; 95% CI: 1.42-2.49), as was each component of NACE (all-cause mortality, HR: 1.77; 95% CI: 1.22-2.55; MI, HR: 1.67; 95% CI: 1.18-2.36; definite/probable stent thrombosis, HR: 1.71; 95% CI: 1.10-2.65; and major bleeding, HR: 1.38; 95% CI: 1.06-1.80). Compared with the CA-AKI–/CKD– group, the CA-AKI+/CKD– (HR: 1.83; 95% CI: 1.33-2.52), CA-AKI–/CKD+ (HR: 1.56; 95% CI: 1.15-2.13), CA-AKI+/CKD+ (HR: 3.29; 95% CI: 1.92-5.67), and maintenance dialysis (HR: 2.67; 95% CI: 1.65-4.31) groups were at higher risk of NACE.
CA-AKI was relatively common after contemporary PCI and was associated with increased 2-year rates of NACE. Patients with pre-existing CKD were at particularly high risk for NACE after CA-AKI.
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