Antiphospholipid syndrome nephropathy in systemic lupus erythematosus.

In the course of the antiphospholipid syndrome (APS), the existence of vaso-occlusive lesions capable of affecting numerous organs is now well established. The renal involvement attributable to primary APS, APS nephropathy (APSN), corresponds to vaso-occlusive lesions of the intrarenal vessels, associating side-by-side, acute thromboses with chronic arterial and arteriolar lesions, leading to zones of cortical ischemic atrophy. A retrospective study of 114 lupus patients undergoing renal biopsy was undertaken to determine the following: (1) if APSN can be found in the course of systemic lupus erythematosus (SLE); (2) if certain clinical and biologic factors can permit the prediction of the presence of APSN; and (3) if APSN is a superadded renal morbidity factor in lupus patients. This study shows the following: (1) APSN occurs in SLE (32% of patients with renal biopsies) in addition to, and independently of, lupus nephritis; (2) APSN is statistically associated with lupus anticoagulant but not with anticardiolipin antibodies; (3) APSN is associated with extrarenal APS, mainly arterial thromboses and obstetrical fetal loss, but not with the venous thromboses of APS; (4) APSN is an independent risk factor, over and above lupus nephritis, that contributes to an elevated prevalence of hypertension, elevated serum creatinine, and increased interstitial fibrosis. Thus, it seems likely that, because of its associations with hypertension, elevated serum creatinine, and increased interstitial fibrosis, APSN may worsen the prognosis in these patients. APSN may also have therapeutic significance in that its recognition should permit a better balance between immunosuppressor and antithrombotic and/or vasoprotective therapy. Finally, this study suggests that APSN should be considered as an element to be included in the classification criteria of APS.     

系统性红斑狼疮并发继发性抗磷脂综合征肾损害11例临床病理分析

目的 分析系统性红斑狼疮（SLE）并发继发性抗磷脂综合征（APS）肾损害的临床病理表现,旨在提高对该类疾病的认识。 方法 回顾性分析北京协和医院2000年至2010年期间确诊SLE并发继发性APS（SLE伴APS）并行肾组织学检查的11例患者的资料,分析其临床病理特点,并比较其和SLE不伴APS患者在肾损害的临床病理及预后上的差异。 结果 11例SLE伴APS患者均有肾脏受累,突出表现为高血压（54.5%）、大量蛋白尿（≥3.5 g/d）（72.7%）和肾功能异常（45.5%）。SLE伴APS患者的舒张压、平均动脉压以及肾小球滤过率（eGFR）均明显高于SLE不伴APS患者（均P < 0.05）。8例（72.7%）SLE伴APS患者存在肾内血管的“血管闭塞性表现”,即符合抗磷脂综合征肾病（APSN）的病理表现,包括肾小血管、肾小球毛细血管血栓形成以及肾小动脉内膜增生、局灶性肾皮质萎缩、肾小管甲状腺样化,其中慢性APSN表现5例（45.5%）,急性APSN表现4例（36.4%）（其中1例同时有急性和慢性表现）;其APSN的发生率以及急性APSN的发生率明显高于SLE不伴APS患者（P < 0.05）。 结论 SLE并发APS肾损害患者除狼疮肾炎外,多并发APSN,临床上高血压和肾功能异常更为突出。     

抗磷脂综合征的肾损害

目的分析抗磷脂综合征(APS)致肾损害的临床特点,旨在提高对该类疾病的认识。方法回顾性分析北京协和医院1983年至2004年期间91例APS中肾损害的临床特点及其中8例的肾组织学表现。结果原发性APS(PAPS)13例(14.3%);继发性APS(SAPS)78例(85.7%),其中系统性红斑狼疮(SLE)55例(占SAPS的70.5%)。APS伴肾损害共82例(90.1%),男性20例、女性62例;PAPS肾损害发生率为76.9%,SAPS为92.3%;发生肾损害时年龄为(38±14)岁,肾损害前病程为(4.9±6.8)年。肾损害临床表现主要为蛋白尿(92.7%)、肉眼血尿(2.4%)、镜下血尿(76.8%)、高血压(33.0%)、肾功能不全(18.3%),其中12.2%为肾病综合征。14例(15.4%)出现急性肾功能不全,病因包括血栓性微血管病、肾动脉栓塞、肾静脉血栓形成等。肾组织学检查8例,均为SLE所致PAPS,APS肾病占62.5%,表现为肾小血管、肾小球毛细血管血栓形成以及肾小叶间动脉内膜增生、洋葱皮样改变。结论APS肾损害比较常见,临床上以蛋白尿最为多见,可伴血尿、高血压,可引起血栓性微血管病、肾动脉栓塞或肾静脉血栓形成,致肾功能急剧恶化。     

Case of primary antiphospholipid antibody syndrome with repeated renal biopsies

Antiphospholipid antibody syndrome (APS) is characterized by the presence of repeated arterial and venous thrombosis, recurrent fetal loss and thrombocytopenia. Recently, renal involvement associated with APS is being increasingly recognized and discussed. In most cases, there has been a vascular nephropathy characterized by small vessel vaso-occulusive lesions associated with fibrous intimal hyperplasia of the interlobular arteries, thrombosis and focal cortical atrophy. We report a case of a 38-year-old patient with primary APS. Renal biopsies were performed three times in 26 years. Various glomerular and vascular lesions associated with APS were observed and discussed.     

Kidney disease associated with primary antiphospholipid syndrome: clinical signs and histopathological features in an case experience of five cases

BACKGROUND: The primary antiphospholipid syndrome (PAPS) is characterized by the presence of circulating antiphospholipid antibodies, clinically associated with blood hypercoagulability. Renal involvement in course of PAPS is very frequent, although the true prevalence of PAPS-correlated kidney disease is difficult to estimate. MATERIALS AND METHODS: We reviewed 270 consecutive renal biopsies examined in our Nephrology Division of Bari University Hospital between 1998 and 2004 to identify those performed in patients with PAPS. RESULTS: We identified five biopsies performed in patients with PAPS. In three patients the diagnosis of PAPS was made at onset of the kidney disorder, while in the other two cases the initial diagnosis was primary focal segmental glomerulosclerosis (FSGS). In these cases the subsequent finding of positive antiphospholipid antibodies reoriented the diagnosis toward PAPS-correlated nephropathy. The clinical onset of kidney disease consisted of acute renal failure in three patients and urinary abnormalities in the other two. Histological examination of renal biopsies showed vascular lesions (intimal fibrous hyperplasia, arteriolar hyalinosis, double outline of the capillary walls) in four patients. Focal segmental glomerulosclerosis was present in four patients, two of whom showed double outline of the capillary walls. All patients had tubulo-interstitial lesions, while immunofluorescence was positive in only two patients. All patients preserved stable renal function throughout follow-up (mean value: 10.6 years, range 4 months-24 years). The prevalence of PAPS-correlated nephropathy in our population was 1.85% CONCLUSION: Our data confirm that PAPS-associated nephropathy has slow progression and rarely leads to end-stage renal failure. The prevalence of PAPS-correlated nephropathy is likely underestimated because some patients with a diagnosis of primary focal sclerosis may actually be affected by PAPS.     

Renal thrombotic microangiopathy in patients with systemic lupus erythematosus and the antiphospholipid syndrome.

Current studies indicate that a thrombotic microangiopathy (TMA) identifies patients with systemic lupus erythematosus (SLE) who are at high risk of progressing to end-stage renal disease. We have observed two patients with SLE and one patient with a primary antiphospholipid syndrome (APS) who developed acute renal insufficiency with thrombocytopenia. Renal biopsies showed a TMA characterized by thrombi or by cellular and mucoid intimal hyperplasia of small arteries and arterioles. No arterial or arteriolar immune-complex deposits were detected by immunofluorescent or electron microscopy. Biopsies from one SLE patient and the APS patient showed no immune-complex glomerular disease. Both had serum antiphospholipid antibodies (aPL). aPL were not detected in the serum of the other SLE patient who had an active lupus nephritis. Acute renal failure and thrombocytopenia resolved in each case following treatment by plasmapheresis or prednisone and heparin. None of the patients were initially treated with cytotoxic drugs. As more knowledge is gained, the accurate identification of renal vascular lesions in SLE or related diseases could influence renal prognosis and choice of therapy. The cases reported here provide further evidence that a TMA can cause acute renal failure independent of lupus nephritis. TMA should be distinguished from other forms of renal vascular disease, particularly a noninflammatory lupus microangiopathy, which is probably mediated by subendothelial immune-complex deposits. The absence of immunoglobulin deposits in vessels involved by a TMA indicates that microvascular thrombosis is promoted by mechanisms other than those usually attributed to immune-complex disease. Phospholipid reactive antibodies may be pathogenetic in some cases.     

Primary antiphospholipid antibody syndrome and mesangial IgA glomerulonephritis

The antiphospholipid antibody syndrome (APS) is characterized by recurrent thrombosis, fetal loss, multiorgan involvement, and the presence of lupus anticoagulant and/or anticardiolipin antibody. When not associated with systemic lupus erythematosus, other collagen diseases, or ingestion of medications, the condition is called primary APS. The kidney may be involved in the APS syndrome with acute nephritis and renal failure. The cases with renal biopsy studies have shown variable glomerular morphology, ranging from mild mesangial changes to a diffuse endocapillary proliferative glomerulonephritis. The most frequent lesion is thrombotic microangiopathy or features seen in the hemolytic uremic syndrome. Apart from fibrin thrombus deposition, only a few cases have shown focal and segmental deposits of IgG and/or IgM and/or C3. We describe a patient with primary APS who had thrombosis with lower limb amputation and acute renal failure. The renal biopsy specimen showed a focal proliferative glomerulonephritis with endothelial proliferation and damage, with diffuse heavy mesangial deposits of IgA and fibrinogen. This case with diabetes mellitus, but without diabetic nephropathy, represents the occurrence of primary APS and mesangial IgA nephropathy which potentiated the renal injury, leading to acute renal failure. The relationship to the Henoch-Sch?nlein syndrome is discussed.     

Is it possible to diagnose primary anti-phospholipid syndrome (PAPS) on the basis of renal thrombotic microangiopathy (PAPS nephropathy) in the absence of other thrombotic process?

The kidneys are a major target of PAPS. The histologic lesions of PAPS nephropathy are vascular; among them thrombotic microangiopathy (TMA) is the most characteristic. It is still not clear in the literature whether the nephropathy can be the unique manifestation of PAPS in the absence of other thrombotic processes; that is: do the renal microthrombotic lesions allow to make the diagnosis of PAPS in presence of anti-phospholipid antibodies (APA)? With this purpose we present three clinical cases. The first patient had severe hypertension C4 hypocomplementemia, thrombocytopenia, and mitralic valve insufficiency. LAC and anti-cardiolipin antibodies at high titre were positive. The histologic picture was characterized by basement membrane reduplication and arteriolar mucoid degeneration, which are features of early phase of TMA. The second patient had severe hypertension. The detection of anti-cardiolipin antibodies was performed several times and resulted positive three times, four months after the diagnosis as well. The renal histologic features were consistent with late lesions of TMA. The third patient had severe hypertension, rapidly progressive renal failure, tricuspidal valve insufficiency and two positive anti-phospholipid antibodies determinations three weeks apart (in two occasions anti-cardiolipin and in one occasion LAC as well were found). The renal lesions were characteristic for TMA. In conclusion we think that patients with TMA and antiphospholipid antibodies can be considered affected by PAPS, as the thrombotic process is represented by thrombosis in preglomerular arterioles, which leads to TMA.     

Silent renal disease in systemic lupus erythematosus

Several recent studies have focused on the discrepancy between lupus nephropathy and clinical renal involvement and, consequently, question the relevance of renal biopsy in these patients. We analyze the clinical characteristics, histological renal findings and subsequent course of patients with silent renal disease. Renal biopsy was performed in 15 patients with systemic lupus erythematosus (SLE) who had no clinical signs of renal involvement (no urinary sediment abnormalities, absence of proteinuria and serum creatinine less than 1.3 mg/dl). All biopsies were classified according to a modified classification proposed by the WHO. Six cases (40%) showed no histological or immunofluorescence changes (type I), 7 (47%) had mesangial nephropathy (3 type IIa and 4 type IIb) and 2 (13%) had focal proliferative glomerulonephritis (type III). None of the patients had previous evidence of neurological abnormalities. Patients with type I only had arthritis, skin lesions and Raynaud's phenomenon. By contrast, 7 patients with histological renal involvement had serositis or hemolytic anemia. All cases with silent nephropathy were treated with steroids and showed a benign clinical course with stable renal function and absence of urinary abnormalities during follow-up. We concluded that in the absence of clinical renal abnormalities, renal involvement is not uncommon in SLE. We believe that a renal biopsy should be performed mainly in those SLE patients presenting with clinical manifestations other than arthritis or cutaneous lesions since this policy may allow detection of significant silent renal injury.     

Is It Possible to Diagnose Primary Anti-phospholipid Syndrome (PAPS) on the Basis of Renal Thrombotic Microangiopathy (PAPS Nephropathy) in the Absence of Other Thrombotic Process?

The kidneys are a major target of PAPS. The histologic lesions of PAPS nephropathy are vascular; among them thrombotic microangiopathy (TMA) is the most characteristic. It is still not clear in the literature whether the nephropathy can be the unique manifestation of PAPS in the absence of other thrombotic processes; that is: do the renal microthrombotic lesions allow to make the diagnosis of PAPS in presence of anti-phospholipid antibodies (APA)? With this purpose we present three clinical cases. The first patient had severe hypertension C4 hypocomplementemia, thrombocytopenia, and mitralic valve insufficiency. LAC and anti-cardiolipin antibodies at high titre were positive. The histologic picture was characterized by basement membrane reduplication and arteriolar mucoid degeneration, which are features of early phase of TMA. The second patient had severe hypertension. The detection of anti-cardiolipin antibodies was performed several times and resulted positive three times, four months after the diagnosis as well. The renal histologic features were consistent with late lesions of TMA. The third patient had severe hypertension, rapidly progressive renal failure, tricuspidal valve insufficiency and two positive anti-phospholipid antibodies determinations three weeks apart (in two occasions anti-cardiolipin and in one occasion LAC as well were found). The renal lesions were characteristic for TMA. In conclusion we think that patients with TMA and anti- phospholipid antibodies can be considered affected by PAPS, as the thrombotic process is represented by thrombosis in preglomerular arterioles, which leads to TMA.     

Membranous nephropathy with crescents

Membranous nephropathy is a common cause of nephrotic syndrome in adults and can be primary or secondary to systemic lupus erythematosus, chronic infection, or drugs. Rapid decline in renal function in patients with membranous nephropathy may be due to renal vein thrombosis, malignant hypertension, or an additional superimposed destructive process involving the renal parenchyma. Crescents are rare in primary membranous nephropathy and thus suggest another underlying disease process, such as combined membranous and focal or diffuse lupus nephritis. However, in some patients with membranous nephropathy and crescents, the crescentic lesion may be due to a distinct, separate disease process, such as anti-glomerular basement membrane antibodies or anti-neutrophil cytoplasmic antibodies-related pauci-immune glomerulonephritis. Here we describe a case with such renal biopsy findings, review previous reported cases, and discuss possible implications for pathogenesis of the coexistence of these lesions.     

Epidemiologic data of renal diseases from a single unit in China: analysis based on 13,519 renal biopsies

Renal biopsy specimens of 13,519 cases were collected during the period of January 1979 to December 2002 from the Research Institute of Nephrology, Nanjing University School of Medicine, Nanjing, China. Analysis of the data of this group of patients showed that primary glomerulonephritis (GN) remained the most important and prevalent renal disease in China. The ratio of primary to secondary GN was 2.75:1. However, it is declining progressively in the past two decades with an increment in the incidence of diabetic nephropathy and nephrosclerosis. IgA nephropathy (IgAN) constituted 45.26% of the primary GN, while non-IgA mesangial proliferative lesions were 25.62%. Membranous nephropathy was 9.89% and minimal change disease was 0.93%, remarkably less. The most prevalent etiology of secondary GN was systemic lupus erythrematosus (SLE) (54.3%) followed by Henoch-Sch?nlein purpura (20.3%), diabetic nephropathy (6.6%), systemic vasculitides (4.0%), and amyloidosis (2.2%). Based on the study of biopsy materials obtained from 607 cases manifesting chronic renal failure, IgAN was identified as the most frequent cause (26.69%) of chronic renal failure.     

Clinicopathological study of originally non-lupus “full-house” nephropathy

Background: Glomerular “full-house” immunofluorescence staining commonly indicates lupus nephritis. However, some non-lupus nephropathy also can present with a “full-house” immunofluorescence pattern mimicking lupus nephritis. The goal of this study is to define the clinicopathological spectrum of originally non-lupus “full-house” nephropathy. Methods: Records of 24 patients with “full-house” nephropathy in the absence of clinical or serological evidence of systemic lupus erythematosus (SLE) at the time of renal biopsy were abstracted for demographics, clinical presentation, laboratory data, renal biopsy findings, and clinical follow-up. Results: The clinicopathological diagnoses included membranous glomerulonephritis (GN) (46%), IgA nephropathy (21%), membranoproliferative GN (12.5%), postinfectious GN (12.5%), C1q nephropathy (4%), and unclassified mesangial GN (4%). No one had endothelial tubuloreticular inclusions. One patient originally diagnosed as IgA nephropathy developed anti-DNA antibody and another one patient with membranous GN developed hypocomplementemia 8 months and 10 months after renal biopsy, respectively. The two patients also developed clinical symptoms of lupus subsequently. Conclusions: There was a broad spectrum of glomerular histological findings in non-lupus “full-house” nephropathy. The possibility of “full-house” nephropathy preceding the emergence of overt systemic lupus erythematosus remained to be elucidated.     

Reflux nephropathy: a clinico-pathological study of 16 cases

The pathologic features of 16 nephrectomy specimens obtained from patients with a radiological diagnosis of reflux nephropathy were analyzed. Chronic pyelonephritis was diagnosed in 7 cases, renal dysplasia in 5 and segmental atrophy in 4. Clear correlations between pathologic pictures and pathogenic mechanisms involved in the development of renal lesions in kidneys with reflux are difficult to establish. These results show, however, that 'reflux nephropathy' is a broad term, which encompasses both congenital and acquired renal lesions.     

Two cases of systemic lupus erythematosus accompanied by antiphospholipid syndrome nephropathy without immune complex nephritis

We report here two interesting cases of systemic lupus erythematosus(SLE) accompanied by antiphospholipid syndrome nephropathy(APSN). These cases satisfied the criteria for SLE established by the American College of Rheumatology 1997 and also satisfied the criteria for antiphospholipid syndrome (APS) established by the Sapporo International Workshop of APS 1998. Both cases had high blood pressure with elevated plasma renin activity, proteinuria and renal dysfunction. Their biopsied renal specimens showed the characteristic findings for APSN, such as mesangial proliferation, double contours, thickening of the capillary loops, and intimal hyperplasia, but there was no evidence for immune complexes in the glomeruli, which were examined by the indirect immunofluorescence methods and the electron microscopy method. These results indicated that their renal dysfunction was caused by APSN, but not by immune complex nephritis. In addition to treatment with prednisolone, they were administered anticoagulants(warfarin, or aspirin, or heparin) for APSN and an angiotensin II receptor blocker, candesartan, for the hypertension. Subsequently, their conditions recovered with the improvement of renal function and hypertension. Our experiences suggest that anticoagulant therapy in addition to corticosteroids offers advantages in the treatment of patients with SLE accompanied by APSN and renal dysfunction.     

Prevalence and clinicopathologic findings of antiphospholipid syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies

AIM: To determine the prevalence of antiphospholipid syndrome nephropathy (APSN) in Thai systemic lupus erythematosus (SLE) patients who underwent renal biopsy and to compare the relationship of renal histopathology and other significant clinical parameters between SLE patients with and without APSN. METHODS: A retrospective analysis was undertaken in systemic lupus erythematosus patients (n = 150, 44 <15 years old, 106 0e;15 years old) who underwent renal biopsy. The specimens were evaluated for histological features of APSN and other significant clinical parameters. The result of antiphospholipid antibodies, clinical course, and renal function from chart review were analysed. RESULTS: The prevalence of APSN in systemic lupus erythematosus patients who underwent renal biopsies was 34% (16% in <15-year-old group, 41.5% in > or =15-year-old group). APSN was associated with more severe hypertension (P = 0.002 for systolic and P = 0.004 for diastolic blood pressure), acute renal failure (P = 0.003), persistent heavy proteinuria (P < 0.001 for 4+ proteinuria), severe lupus nephritis (class III and IV, P = 0.014, high activity and chronicity indices, P < 0.001) and a tendency to progress to end-stage renal disease. CONCLUSION: Systemic lupus erythematosus patients who underwent renal biopsies in our institute showed a prevalence of APSN comparable to those in western countries. The presence of APSN was significantly higher in the adult than in the paediatric population. Its association with poor prognostic indicators suggests poor renal outcome. Clinicians should be aware of this condition in order to give proper care to systemic lupus erythematosus patients.     

Prognosis of lupus membranous nephropathy in children

The occurrence of membranous nephropathy in pediatric series of systemic lupus erythematosus has been reported only rarely, probably due to a very low frequency. One hundred fifty-four children who were seen in 100 French pediatric centers between January 2002 and April 2005 were included. Fifteen (12 girls and three boys) out of the 81 (18.5 %) children with renal involvement presented histological features of membranous nephropathy. Their ages ranged from six to 15 years old (mean=11.3) at the age of SLE diagnosis and 8/15 children were of African origin. Isolated membranous nephropathy was observed in nine patients, of whom five patients displayed a complete recovery following immunosuppressive treatment. Associated proliferative lesions were observed on the first kidney specimen in two patients and in a further renal biopsy in four other patients, leading to a less favorable course of lupus nephropathy.     

Severe Vascular Lesions and Poor Functional Outcome in Kidney Transplant Recipients with Lupus Anticoagulant Antibodies

The impact of antiphospholipid antibodies (APA) on clinical outcome and graft histology following renal transplantation remains poorly known and controversial. We retrospectively explored the functional and histological significance of APA, primarily lupus anticoagulant (LA), in kidney transplant recipients using a systematic evaluation of 3‐ and 12‐month posttransplant screening biopsies and glomerular filtration rate measurements (mGFR). During the study period, 37 patients had APA (2.7%), primarily LA, and 12 fulfiled antiphospholipid syndrome (APS) diagnostic criteria (0.8%) at the time of transplantation. Early after transplantion, 4 of the 12 APS patients died. Early thrombosis of graft vessels and deep venous thrombosis occurred more frequently in APA+ patients than in controls (27% vs. 7%, p < 0.05 and 35% vs. 14%, p < 0.05, respectively). The survival rate was significantly lower in patients with APS. Strikingly, the hallmark lesions of APS‐associated nephropathy (APSN) were found in most of screening graft biopsies in APA+ patients but not in the controls. Accordingly, APA+ patients had a dramatic increase in chronic vascular scores and a faster decline in mGFR at 1 year. In conclusion, renal transplantation may be life‐threatening in APS patients, and the presence of LA at the time of transplantation is associated with a high rate of allograft APSN and poor transplantation outcomes.     

A single chinese center investigation of renal artery stenosis in 141 consecutive cases with coronary angiography

BACKGROUND: There is an increasing prevalence of ischemic nephropathy in the aging population of the world. However, the exact incidence of ischemic nephropathy in the Chinese population is still uncertain. The present study investigated the incidence of renal artery stenosis (RAS) in patients with suspected coronary artery disease (CAD) using renal angiography. METHODS: Renal angiography was performed immediately after coronary artery angiography in 141 patients with suspected CAD, including 59 males and 82 females whose mean ages were 59 +/- 10 years. Comorbidities included hypertension (n = 69), diabetes mellitus (n = 21), hyperlipidemia (n = 19), hypokalemia (n = 7) and preoperative renal insufficiency (Cr >132 micromol/l; n = 14). The patients were divided into CAD (luminal narrowing of > or =50%) and non-CAD (luminal narrowing of <50%) subgroups, and RAS (luminal narrowing of > or =50%) and non-RAS subgroups. In the RAS group, there were 11 patients (5 males, 6 females) in whom percutaneous transluminal renal angioplasty was performed in conjunction with stent implantation due to refractory hypertension. RESULTS: The incidence of RAS was 18.4% (26/141) in all cases and 30.8% (16/52) in patients with CAD identified by coronary artery angiography. Ten cases with RAS were found among the 89 cases with normal coronary arteries (11.2%). The incidence of RAS in patients with CAD was higher than that in patients without CAD (30.8 vs. 11.2%, p< 0.05). In 52 cases with CAD, the incidence of RAS with three vessel lesions was significantly higher than that with one or two vessel lesions. Hypertension, CAD, renal insufficiency, hyperlipidemia and hypokalemia were associated with a higher risk of RAS. CONCLUSIONS: This study suggests that RAS is very common in the elderly Chinese population, specifically for those with three vessel lesions in CAD. For early detection of potential ischemic nephropathy, renal angiography is necessary in patients who receive coronary artery angiography.