The following represent additions to UpToDate since the last version of What’s New that were considered by the authors and editors to be of particular interest.
GLOMERULAR DISEASE AND VASCULITIS
Mycophenolate mofetil versus azathioprine for lupus nephritis — The ALMS Maintenance Trial was a multinational study in which 227 patients who had achieved remission with either mycophenolate mofetil (MMF) or cyclophosphamide were randomly assigned to MMF (1 g twice daily) or azathioprine (2 mg/kg per day) as maintenance therapy for 36 months [1]. Among patients who responded to induction therapy with either MMF or cyclophosphamide, treatment failure at 36 months (defined by renal relapse, the need to intensify therapy, doubling of the serum creatinine, or death) was significantly lower with MMF compared with azathioprine groups. (See "Therapy of diffuse or focal proliferative lupus nephritis", section on 'Azathioprine versus mycophenolate mofetil'.)
Thromboembolic events and membranous nephropathy — The risk of thromboembolic events was assessed among 898 patients with membranous nephropathy who were identified from the Glomerular Disease Collaborative Network and the Toronto Glomerulonephritis Registry [2]. Clinically evident and radiologically confirmed venous thromboembolic events occurred in 7.2 percent of patients and most events occurred within the first two years of diagnosis. A low serum albumin concentration at the time of diagnosis, but not the degree of proteinuria, predicted a venous thromboembolic event. (See "Treatment of idiopathic membranous nephropathy", section on 'Anticoagulation' and "Renal vein thrombosis and hypercoagulable state in nephrotic syndrome", section on 'Epidemiology'.)
Cocaine and levamisole in ANCA-associated vasculitis — Approximately 70 percent of cocaine bought illicitly in the United States is contaminated or “cut” with levamisole, an immunomodulatory agent. In the largest published series, 30 patients with cocaine and levamisole-related ANCA-associated vasculitis are described [3]. The most common clinical manifestations included arthralgias (83 percent) and skin lesions (61 percent). All patients had a positive MPO-ANCA and 50 percent had positive PR3-ANCA. An abnormal urinalysis (including either proteinuria, hematuria or cellular casts) was present in 8 patients. (See "Clinical spectrum of antineutrophil cytoplasmic antibodies", section on 'Cocaine and levamisole'.)
ACUTE AND CHRONIC KIDNEY DISEASE
Sodium intake and progression to end-stage renal disease — A high sodium diet was associated with both a blunting of the proteinuria reduction induced by the ACE inhibitor ramipril and a higher incidence of end-stage renal disease (ESRD) in proteinuric patients with chronic kidney disease enrolled into the REIN and REIN-2 trials [4]. Compared with those consuming a low sodium diet (less than 125 mmol/day), patients on a high sodium diet (greater than 250 mmol/day) had a smaller reduction in proteinuria in response to ramipril therapy (20 versus 31 percent), and a higher incidence of ESRD (32 versus 16 percent). (See "Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults", section on 'Importance of salt intake'.)
Microvascular complications in type 1 diabetes — In the Epidemiology of Diabetes Interventions and Complications (EDIC) follow-up study to the Diabetes Control and Complications Trial (DCCT), intensive insulin therapy compared with conventional therapy for 6.5 years during the DCCT significantly reduced the risk of developing impaired renal function over a median follow-up period of 22 years [5]. This decreased risk occurred despite an absence of a difference in A1C values during the post-DCCT trial period. This phenomenon has been called "metabolic memory." (See "Glycemic control and vascular complications in type 1 diabetes mellitus", section on 'Nephropathy'.)
APOL1 and early renal disease in African Americans — Two separate disease-causing polymorphisms in the apolipoprotein L1 (APOL1) gene found exclusively in African Americans and inherited as autosomal recessive traits confer a substantially higher risk of ESRD. In addition, APOL1 mutations are associated with an earlier onset of kidney disease. In a study of 407 African American patients receiving hemodialysis, patients with two mutant alleles were significantly younger at the time of dialysis initiation than those without any disease-causing APOL1 mutation (49 versus 62 years) [6]. In a large population based study that included 1776 African Americans without known kidney disease (mean age 45 years), homozygotes for APOL1 mutations were more likely to have microalbuminuria (18 versus 9 percent) and an estimated glomerular filtration rate below 60 mL/min per1.73 m2 (6 versus 3 percent) compared with other individuals [7]. (See "Epidemiology of chronic kidney disease", section on 'APOL1 in African Americans'.)
Tolvaptan therapy for autosomal dominant polycystic kidney disease — Therapy with the vasopressin receptor antagonist tolvaptan may limit kidney enlargement and slow renal function decline in patients with autosomal dominant polycystic kidney disease (ADPKD). In a study that compared 63 patients enrolled in two uncontrolled, open label trials of tolvaptan therapy with untreated but otherwise similar patients from historical cohorts, tolvaptan therapy was associated with significantly smaller increases in total kidney volume (1.7 versus 5.8 percent), and slower annual declines in estimated glomerular filtration rate (0.71 versus 2.1 mL/min per 1.73 m2) [8]. (See "Course and treatment of autosomal dominant polycystic kidney disease", section on 'Vasopressin receptor antagonists'.)
Pregnancy risks in mild to moderate CKD — Women with mild to moderate CKD have worse maternal and fetal outcomes. In a meta-analysis of 13 cohort studies, pregnant women with preexisting renal impairment were significantly more likely than women with normal renal function to develop gestational hypertension, preeclampsia, eclampsia, or to die (12 versus 2 percent) [9]. Maternal mortality was more frequent in those with CKD (4 versus 1 percent), although this was not statistically significant. Premature birth was significantly higher among women with renal impairment (13 versus 6 percent), while nonsignificantly higher rates were noted for intrauterine growth restriction, small for gestational age and stillbirth. (See "Pregnancy in women with underlying renal disease", section on 'Pregnancy in mild to moderate CKD'.)
RenalGuard system may decrease contrast nephropathy — The RenalGuard system is a fluid management device that guides fluid replacement by providing a real-time display of urine and replacement fluid volumes. Two studies have suggested that furosemide-induced diuresis and matched saline infusion that is guided by the RenalGuard system may decrease the risk of contrast nephropathy among high risk patients undergoing angiography [10,11].
(See "Prevention of contrast-induced nephropathy", section on 'RenalGuard system'.)
Acetylcysteine and contrast nephropathy — The Acetylcysteine for the prevention of Contrast-induced Nephropathy (ACT) trial showed no benefit over placebo of acetylcysteine (1200 mg orally twice daily) on the incidence of contrast nephropathy among 2308 high-risk patients who were undergoing angiography [12]. The trial was underpowered to exclude a potential benefit of acetylcysteine among patients with severe kidney insufficiency. (See "Prevention of contrast-induced nephropathy", section on 'Acetylcysteine'.)
Treatment of hyperparathyroidism in CKD — In a randomized open-label trial that included 80 patients with CKD (estimated GFR 15 to 60 mL/min per 1.73m2) paricalcitol was more effective than ergocalciferol in reducing parathyroid hormone levels at 16 weeks [13]. The rates of hypercalcemia and hyperphosphatemia were not different between groups. (See "Management of secondary hyperparathyroidism and mineral metabolism abnormalities in adult predialysis patients with chronic kidney disease", section on 'Active vitamin D analogues'.)
DIALYSIS
Predictors of sudden death — Predictors of sudden cardiac death among hemodialysis patients were evaluated using data from the HEMO study [14]. Among 1745 enrolled hemodialysis patients, there were 808 deaths over 2.5 years, 22 percent of which were due to sudden cardiac death. Age, diabetes, peripheral vascular disease, ischemic heart disease, a low serum creatinine (reflecting decreased muscle mass and poor nutrition) and an elevated alkaline phosphatase predicted a higher risk for sudden cardiac death. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in dialysis patients", section on 'Risk factors and causes'.)
TRANSPLANTATION
Calcineurin inhibitors and renal allograft failure — A meta-analysis that included 17 studies (4131 patients) showed that calcineurin inhibitor-minimizing regimens were associated with reduced overall graft failure and death-censored graft failure with no difference in graft failure secondary to rejection [15]. (See "Chronic renal allograft nephropathy", section on 'Changes in calcineurin inhibitor exposure'.)
NEPHROLITHIASIS
Use of stents in conjunction with ureteroscopy — Stents are often placed after ureteroscopy lithotripsy in an effort to prevent obstruction and pain. A meta-analysis of 16 randomized trials involving 1573 patients evaluated the benefits of stent placement after ureteroscopy [16]. Compared with those who did not receive a stent, patients receiving stents had significantly longer operative times, and more pain and lower urinary tract symptoms (dysuria, frequency or urgency, and hematuria), while there was no difference in stone free rate, fever, urinary tract infection, requirement for analgesia, urinary strictures, or unplanned rehospitalization. Thus, routine placement of stents after uncomplicated ureteroscopy should be discouraged. (See "Options in the management of renal and ureteral stones in adults", section on 'Indications for stent placement'.)
All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.
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