Shorter Renal Survival Research Articles

Clinical characteristics and outcomes of MPO-ANCA-associated glomerulonephritis with bronchiectasis: A retrospective case-control study

BackgroundThe association of bronchiectasis with myeloperoxidase (MPO) antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (MPO-AAV) has been widely described in recent studies. However, the clinical features and outcomes of MPO-ANCA-associated glomerulonephritis (MPO-ANCA GN) patients with bronchiectasis remain enigmatic. MethodsMPO-ANCA GN patients with bronchiectasis were compared to MPO-ANCA GN patients alone. Clinical imaging, pathological tests, and follow-up examination data of patients were collected retrospectively. Progression to end-stage renal disease (ESRD) and death was treated as endpoint events. Results153 cases (52 patients with bronchiectasis) were included in this study. Compared to MPO-ANCA GN patients alone, MPO-ANCA GN patients with bronchiectasis exhibited a lower level of proteinuria (p = 0.019) and relatively higher eGFR level. MPO-ANCA GN patients with bronchiectasis had less frequent incidences of interstitial lung disease (ILD) and emphysema (p<0.001, p = 0.016, respectively) but with higher rates of pulmonary infection (p<0.001). Bronchiectasis severity (the modified Reiff score) was positively correlated with MPO antibody titers (ρ=0.480, p<0.001), but not with shorter renal survival. A relatively higher remission rate was been seen in MPO-ANCA GN patients with bronchiectasis, who showed reduced susceptibility in progressing to ESRD in multivariate analysis (p = 0.043, HR=0.542, 95% CI 0.299–0.982). One-and three-year overall survival rates were 88.2% and 77.3% for MPO-ANCA GN with bronchiectasis cases versus 83.7% and 67.2% for MPO-ANCA GN patients alone (p = 0.431, p = 0.241, respectively). ConclusionThe severity of bronchiectasis was correlated with anti-MPO antibody titers in MPO-ANCA GN patients. For MPO-ANCA GN patients, bronchiectasis associated with good renal prognosis, but it did not improve overall survival.

MO285CLINICAL PRESENTATION OF IGA NEPHROPATHY AND LONG-TERM RENAL OUTCOME

Abstract Background and Aims There is a wide range of clinical presentation of IgA nephropathy (IgAN), from asymptomatic microscopic hematuria to rapidly progressive glomerulonephritis. However, there is little epidemiologic data on the relationship between the clinical pattern at diagnosis and long-term renal outcome. Method We performed a unicentric retrospective study on 299 consecutive IgAN patients (age 43 [35-56] years, 71% male, eGFR 42.1 [25.2-62.8] mL/min, proteinuria 1.3 [0.6-2.6] g/g creatinine) - kidney biopsy proven - between 2010-2017. Patients were followed until composite endpoint (doubling of serum creatinine, ESKD (dialysis or renal transplant) or death, whichever came first) or end of study (May 2018). Results Patients were followed for a mean of 41 (95%CI 38, 44) months, and 80 (27%) patients experienced the composite endpoint. The most frequent clinical presentation at diagnosis regardless of age was nephritic syndrome (68%), followed by asymptomatic urinary abnormalities (AUA) (19%), macroscopic hematuria (15%), acute kidney injury (AKI) (14%) and nephrotic syndrome (10%). The clinical pattern varied in frequency with age: macroscopic hematuria had a bimodal distribution in the 20- and 60-years groups, AKI was more frequent in the 50 to70 years groups, AUA was more often present in the 30 to 50 years groups (Figure 1). Mean renal survival time for the entire cohort was 70 (95%CI 65, 75) months; patients with AKI (40 (95%CI 27, 54) vs 75 (95%CI 69, 80) months, p&amp;lt;0.001), nephrotic syndrome (42 (95%CI 26, 57) vs 73 (95%CI 67,78 months, p&amp;lt;0.001)) at diagnosis had significantly shorter renal survival time. In multivariate Cox regression analysis adjusted for IgAN progression factors, presence of nephritic syndrome at diagnosis was associated with good renal outcome, while clinical presentation as AKI or nephrotic syndrome were associated with poor renal survival (Table 1). Conclusion Although AKI and nephrotic syndrome are uncommon in IgAN at diagnosis, their presence seems to be associated with poor renal survival.

The extent of tubulointerstitial inflammation is an independent predictor of renal survival in lupus nephritis.

Lupus nephritis (LN) is a major complicationin patients with systemic lupus erythematosus (SLE). Tubulointerstitial injury is an inflammatory process that, if not attenuated, can promote renal damage. Despite this, the current 2003 ISN/RPS "glomerulocentric" classification does not include a score for tubulointerstitialinjury. We sought to establish predictors for tubulointerstitial injury and to determine their influence on renal outcomes. This is a retrospective study of a cohort of 166 patients with biopsy-proven LN diagnosed in a Spanish referral center, with a median follow-up of 86months. Chronic tubulointerstitiallesions were defined as interstitial fibrosis and tubular atrophy (IF/TA), whereas tubulointerstitialinflammation (TII) was defined as an acute interstitiallesion. Activity (0-24) and chronicity (0-12) indices were assigned. Composite outcome, definedas advanced CKD or development of kidney failure. The prevalenceof tubulointerstitiallesions was 69.3%. Eighty-one of the biopsies had features of tubulointerstitial inflammationand only 6 of these81 (7%) patients had moderate/severe tubulointerstitial inflammation. The incidence ofinterstitial fibrosis and tubular atrophywas 56.6%. Renal survival was shorter in patients with moderate/severe as compared with absent/mild interstitial fibrosis and tubular atrophy(median: 15-19years, p = 0.009). In the Cox regression model, the grade ofinterstitial fibrosis and tubular atrophy was independently associated with shorter renal survival (hazard ratio: 3.9, 95% CI 1.4-10.5; p = 0.008) after adjusting for degree of IF/TA and hypertension or diabetes. The extent of tubulointerstitial inflammation emerged as an independent predictor of renal survival after adjusting for the grade ofinterstitial fibrosis and tubular atrophy and co-morbid conditions includinghypertension or diabetes. Regarding disease duration at the time of renal biopsy, no significant association was found between the interstitial fibrosis and tubular atrophygroups. The results reported herein need to be validated in future studies to include also groups of patients who usually have a worse prognosis. Consensus on histological classification is needed to aid in definingprognosis.

The Clinical Impact of Glomerular Immunoglobulin M Deposition in Patients with Type 2 Diabetic Nephropathy

Glomerular immunoglobulin M (IgM) deposition is common in diabetic kidney disease. The clinical implication of IgM deposition in the renal tissues of type 2 diabetes mellitus patients with biopsy-proven diabetic nephropathy remains unclear. One hundred thirty-two patients with type 2 diabetes and biopsy-proven pure diabetic nephropathy were enrolled retrospectively. Clinicopathological features and renal outcomes were compared between patients with and without glomerular capillary IgM deposition. A Cox proportional hazards model was employed to identify the risk factors associated with renal survival. Fifty-two patients had positive linear glomerular capillary IgM staining. Patients with glomerular capillary IgM deposition presented with heavier proteinuria, and lower serum albumin. During 35.5 (12, 107) months of follow-up, patients with glomerular tuft IgM deposition had shorter renal survival than those with negative IgM deposition (39 [23.74, 54.26] versus (vs.) 64 [45.82, 82.18] months, P = 0.01). Patients with glomerular complement 1q (C1q) deposition showed worse renal survival than those lacking glomerular C1q deposition (36 [23.82, 48.18] vs. 60 [50.27, 69.74] months, P = 0.001). Worse renal outcome was observed in patients with glomerular C3 deposition than in those without glomerular C3 deposition (37 [22.43, 51.56] vs. 63 [51.75, 74.25] months, P = 0.001). Multivariate Cox proportional analysis demonstrated that combined glomerular capillary IgM and C1q deposition was an independent predictor of end-stage renal disease (hazard ratio 3.75, 95% CI[ 1.68,8.35], P = 0.001). Patients with diabetic nephropathy and combined glomerular capillary IgM and C1q deposition had unfavorable renal outcome, which indicates that IgM derived from B cells might be involved in diabetic kidney injury.

Predictors of renal outcome in HIV-associated nephropathy.

Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is an important cause of end-stage renal disease among African American patients. This study was performed to study the epidemiology of HIVAN in a predominantly black African population and the impact of highly active antiretroviral therapy and other factors on the development of end-stage renal disease. We retrospectively identified all patients with HIVAN, defined by biopsy or strict clinical criteria, in 8 clinics in the United Kingdom. Baseline renal function, HIV parameters, renal pathological index of chronic damage, and responses to highly active antiretroviral therapy were analyzed, and factors associated with adverse renal outcome were identified. From 1998 through 2004, we studied 16,834 patients, 61 of whom had HIVAN. HIVAN prevalence in black patients was 0.93%, and HIVAN incidence in those without renal disease at baseline was 0.61 per 1000 person-years. After a median of 4.2 years, 34 patients (56%) had developed end-stage renal disease. There were no significant differences in renal function and HIV parameters at baseline, time to initiation of highly active antiretroviral therapy, and rates of HIV RNA suppression between the 20 patients who developed end-stage renal disease >3 months after receiving the HIVAN diagnosis and the 23 patients who maintained stable renal function. However, the index of chronic damage score was significantly higher in those who developed end-stage renal disease (P < .001), and an index of chronic damage score >75 was associated with shorter renal survival (P < .001). Whereas overall patient survival suggested an important benefit of highly active antiretroviral therapy, no additional renal benefit of early initiation of highly active antiretroviral therapy or viral suppression could be demonstrated in this large cohort of patients with established HIVAN. Severity of chronic kidney damage, as quantified by biopsy, was the strongest predictor of renal outcome.