ライフサイエンスコーパス: nephropathy

1 range of kidney diseases, including diabetic nephropathy.

2 evels in human and animal models of diabetic nephropathy.

3 ibitors did not slow progression of diabetic nephropathy.

4 herapeutic potential for NOX-E36 in diabetic nephropathy.

5 rug to the distal ileum in patients with IgA nephropathy.

6 cans and with sickle cell disease-associated nephropathy.

7 ing albuminuria-reducing effects in diabetic nephropathy.

8 fundamental initiating mechanism of oxalate nephropathy.

9 nts beta-cell loss and hyperglycemia but not nephropathy.

10 l models with lupus nephritis and folic acid nephropathy.

11 glomerular filtration rate (GFR) decline and nephropathy.

12 microangiopathy of diabetic retinopathy and nephropathy.

13 the renal proteome in mice with acute folate nephropathy.

14 diabetic nephropathy, and adriamycin-induced nephropathy.

15 ive heart failure, hypertension, or diabetic nephropathy.

16 n the pathogenesis and treatment of diabetic nephropathy.

17 al vascular function in hypertension-induced nephropathy.

18 n-human trials for the treatment of diabetic nephropathy.

19 n the medulla that contribute to sickle cell nephropathy.

20 for BKPyV reactivation and BKPyV-associated nephropathy.

21 s were pursued for the treatment of diabetic nephropathy.

22 s in many investigations of contrast-induced nephropathy.

23 he dose-limiting toxicity was late radiation nephropathy.

24 tions and the role of these AGEs in diabetic nephropathy.

25 h adenine-induced chronic tubulointerstitial nephropathy.

26 critical role in the development of diabetic nephropathy.

27 emerging as a critical mediator of diabetic nephropathy.

28 e pathophysiology of polyomavirus-associated nephropathy.

29 associated with tumefactive brain lesions or nephropathy.

30 erapeutic effects of fenofibrate on diabetic nephropathy.

31 unction associated with hypertension-induced nephropathy.

32 gy, diagnosis, and outcomes of recurrent IgA nephropathy.

33 male gender and presence of retinopathy and nephropathy.

34 meruli of SLE patients compared with control nephropathy.

35 e reduced in patients with advanced diabetic nephropathy.

36 improve clinical manifestations of diabetic nephropathy.

37 f IL-17A was sufficient to suppress diabetic nephropathy.

38 uding 61 with additional viremia and 22 with nephropathy.

39 e major autoantigen in idiopathic membranous nephropathy.

40 thereby upregulating NOX4 in early diabetic nephropathy.

41 processing of miRNAs implicated in diabetic nephropathy.

42 hibitors have been shown to improve diabetic nephropathy.

43 y associated with susceptibility to diabetic nephropathy.

44 nd renal damage during experimental diabetic nephropathy.

45 ivity of urine and blood indicates later BKV nephropathy.

46 sively in the second decade of life in ADCK4 nephropathy.

47 r in the setting of Adriamycin (ADR)-induced nephropathy.

48 tes are important features of HIV-associated nephropathy.

49 s, thyroid dysfunction, and contrast-induced nephropathy.

50 uced albuminuria with atrasentan in diabetic nephropathy.

51 rug, Ezetimibe (EZT) on severity of diabetic nephropathy.

52 e tubular epithelium also during obstructive nephropathy.

53 nts with a hypokalemic-alkalotic salt-losing nephropathy.

54 , we examined the role of IL-17A in diabetic nephropathy.

55 diagnosis of paraprotein-induced crystalline nephropathy.

56 l biopsies from human subjects with diabetic nephropathy.

57 the major autoantigen in primary membranous nephropathy.

58 hildren who are already at risk for diabetic nephropathy.

59 OS formation may be a pathomechanism of COQ2-nephropathy.

60 eath was higher among patients with diabetic nephropathy.

61 ted as a major pathogenic factor in diabetic nephropathy.

62 occasionally associated with development of nephropathy.

63 s assigned salient pathogenetic roles in IgA nephropathy.

64 de, reduced proteinuria in patients with IgA nephropathy.

65 not in line with any other known salt-losing nephropathy.

66 A nephropathy, lupus nephritis, and diabetic nephropathy.

67 erum nephritis as a model of immune-mediated nephropathy.

68 rvention in patients with primary membranous nephropathy.

69 ved ROS in promoting progression of diabetic nephropathy.

70 pha relevant in the pathogenesis of diabetic nephropathy.

71 ation status correlated with the severity of nephropathy.

72 is involved in the pathogenesis of diabetic nephropathy.

73 for a biomarker that predicts progression of nephropathy.

74 nd promote functional improvement in chronic nephropathies.

75 peripheral neuropathy (1.40, 1.19-1.66), and nephropathy (1.35, 1.15-1.58).

76 ive glomerulonephritis (23%) followed by IgA nephropathy (19%) and acute tubular injury (19%).

77 cant difference in survival between diabetic nephropathy (23.8%) and other patients with CKD (59.9%;

78 regular screening for retinopathy, 47.1% for nephropathy, 4.5% for neuropathy, and 5.7% for foot ulce

79 ss the long-term outcome of patients with AA nephropathy (AAN) after kidney transplantation.

80 can Study of Kidney Disease and Hypertension nephropathy (AASK-N) is a tubulopathy, we obtained urine

81 lishes the pathological features of diabetic nephropathy, although it does not affect the hyperglycem

82 A antagonist memantine also reduced diabetic nephropathy, although it was less effective than MK-801.

83 ates of the risk of radiocontrast-associated nephropathy among adult patients hospitalized in the Uni

84 ntly, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited substanti

85 e describe a case of crystalglobulin-induced nephropathy and discuss its pathophysiology and the diff

86 essive therapy and triggers BKPyV-associated nephropathy and graft rejection.

87 mesangial deposition is the hallmark of IgA nephropathy and Henoch-Schonlein purpura, the onset of w

88 expression to tubular cells in acute folate nephropathy and human AKI.

89 alpha(-/-) mice with diabetes or obstructive nephropathy and in PPARalpha(-/-) tubular cells treated

90 self in multiple ways, ranging from indolent nephropathy and inflammation to proteinuria with glomeru

91 inflammation, and apoptosis in acute folate nephropathy and less kidney dysfunction and a lower mort

92 hogenesis of severe diabetic retinopathy and nephropathy and may explain why some individuals with ty

93 6 expression in rats with adriamycin-induced nephropathy and mice with hyperglycemia-induced renal in

94 erapy in patients with idiopathic membranous nephropathy and nephrotic syndrome.

95 acid receptor in the prevention of diabetic nephropathy and obesity-induced renal damage.

96 t 18 years with biopsy-confirmed primary IgA nephropathy and persistent proteinuria despite optimised

97 zed 34 adult patients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on angiot

98 n implicated in the pathogenesis of diabetic nephropathy and renal fibrosis; however, the causative r

99 matrix protein that is increased in diabetic nephropathy and tubulopathy.

100 d glomerulosclerosis (indicators of diabetic nephropathy) and attenuated albumin leakage into the ret

101 microvascular (retinopathy, neuropathy, and nephropathy) and macrovascular (cerebrovascular, coronar

102 ia in two independent mouse models, diabetic nephropathy, and adriamycin-induced nephropathy.

103 erebral infarction with calcium depositions, nephropathy, and hepatopathy.

104 the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attributed ESRD among peop

105 besity, hyperinsulinemia, hepatic steatosis, nephropathy, and infertility.

106 t role in the development of type 1 diabetic nephropathy, and its inhibition could be a promising opt

107 scular morbidity and mortality; retinopathy, nephropathy, and neuropathy; and harms.

108 iated with cumulative burden of retinopathy, nephropathy, and peripheral neuropathy among individuals

109 ollowing: a kidney biopsy with PV associated nephropathy, any urine cytology demonstrating "decoy" ce

110 with end-stage kidney disease caused by IgA nephropathy are transplanted every year, and each of the

111 further strengthen the view of HNF1B-related nephropathy as a mitochondrial disorder in adulthood.

112 osis, asthma, neuropathic pain, and diabetic nephropathy, as well as cancer.

113 lycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher HRs for mortality [1.

114 veloped hyperglycemia, oxidative stress, and nephropathy at age 20 weeks compared with their db/m lit

115 rapy for patients with idiopathic membranous nephropathy at high risk of progression to ESRD.

116 ith risk of severe retinopathy and/or severe nephropathy because they modify an individual's ability

117 Moreover PDE5i attenuated the rise of nephropathy biomarkers, soluble urokinase-type plasminog

118 Deeper analysis on chronic allograft nephropathy biopsy specimens suggested that SNAI1 cytopl

119 was then assessed in human chronic allograft nephropathy biopsy specimens.

120 sy specimens with BK polyomavirus-associated nephropathy (BKPyVAN) and specimens with TCMR.

121 BK virus-associated nephropathy (BKVAN) causes renal allograft dysfunction.

122 polyomavirus (BKV) has been shown to induce nephropathy (BKVN), decreasing graft survival.

123 3%) developed CMV disease or BK infection or nephropathy (BKVN).

124 and an array of pediatric problems including nephropathy, blastoma, gonadal dysgenesis and genital di

125 Hematuria is a cardinal symptom in IgA nephropathy, but its influence on the risk of disease pr

126 in salt-sensitive (SS) hypertension-induced nephropathy, but the molecular mechanisms contributing t

127 jor pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remains incomp

128 locks these effects and improves CNI-induced nephropathy by decreasing renin production in the CDs.

129 ion (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leukocyte infi

130 is of obesity-induced renal lipotoxicity and nephropathy by regulating the liver kinase B1/AMP-activa

131 (SOCS1) regulatory protein protects against nephropathy by suppressing STAT-mediated cell responses

132 infections, such as polyomavirus-associated nephropathy, calcineurin inhibitors (CNI), and genetic f

133 Sickle cell nephropathy can occur in patients with homozygous hemogl

134 to dissect the molecular pathways underlying nephropathy caused by TFV and its more toxic analog, ade

135 target of the autoimmune disease, membranous nephropathy, characterised by production of anti-PLA2R a

136 nd show diminished physiological function in nephropathies characterized by altered tissue stiffness,

137 al nephritis (KIN) is a chronic interstitial nephropathy characterized by tubulointerstitial nephriti

138 e been studied for reducing contrast-induced nephropathy (CIN).

139 nt potential side effect is contrast-induced nephropathy (CIN).

140 In univariate analyses, diabetic nephropathy class was not statistically significant in p

141 methods, including determination of diabetic nephropathy class, as defined by the Renal Pathology Soc

142 Renal function was worse in BKV-nephropathy compared with BKV-negative patients beginnin

143 from the Banff Working Group on Polyomavirus Nephropathy, comprising nine transplant centers in the U

144 Congenital obstructive nephropathy (CON) is the most prevalent cause of pediatr

145 Patients with diabetic nephropathy (DN) and autosomal-dominant polycystic kidne

146 of podocytes is an early feature of diabetic nephropathy (DN) and predicts its progression.

147 lbuminuria and 162 individuals with diabetic nephropathy (DN) from the outpatient clinic at Steno Dia

148 PA-LPAR signaling in development of diabetic nephropathy (DN) has not been studied.

149 rly relevant to the pathogenesis of diabetic nephropathy (DN) in which evidence suggests that metabol

150 Diabetic nephropathy (DN) is a major cause of end-stage renal dis

151 Diabetic nephropathy (DN) is one of vascular complications of dia

152 Diabetic nephropathy (DN) is the leading cause of CKD in the West

153 Diabetic Nephropathy (DN) is the leading cause of end-stage renal

154 Diabetic nephropathy (DN) is the leading cause of ESRD worldwide.

155 Diabetic nephropathy (DN) is the major cause of end-stage renal d

156 t proteases aberrantly expressed in diabetic nephropathy (DN) may be involved in the generation of DN

157 rtant to find better treatments for diabetic nephropathy (DN), a debilitating renal complication.

158 lls (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlyi

159 alyzed specimens from patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membrano

160 Using a murine model of diabetic nephropathy (DN), we performed an unbiased RNA-sequencin

161 h contributes to the development of diabetic nephropathy (DN).

162 f diabetic complications, including diabetic nephropathy (DN).

163 ty-related glomerulopathy (ORG) and diabetic nephropathy (DN).

164 ncluding those with FSGS and type 2 diabetic nephropathy (DN).

165 expression has been associated with diabetic nephropathy (DN).

166 been linked to the pathogenesis of diabetic nephropathy (DN).

167 y of kidney injury in patients with diabetic nephropathy (DN).

168 ory and irreversible progression of diabetic nephropathy (DN).

169 as been used to treat patients with diabetic nephropathy (DN).

170 f2 activation and ROS inhibition in diabetic nephropathy (dNP), the Nrf2 activator bardoxolone failed

171 cal segmental glomerulosclerosis or diabetic nephropathy exhibited diminished H3K27me3 and heightened

172 m patients with IgA nephropathy and diabetic nephropathy exhibited substantial activation of p53 and

173 r 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requirement for

174 e followed a cohort of 112 patients with IgA nephropathy for a mean+/-SEM period of 14+/-10.2 years,

175 IgA nephropathy frequently leads to progressive CKD.

176 In the BKV nephropathy group, urine and blood became BKV positive e

177 lial cells from patients with HIV-associated nephropathy (HIVAN) express HIV-1 transcripts, suggestin

178 N-type calcium channel, Cav2.2, in diabetic nephropathy, however, remains to be clarified.

179 Overall, both AT and EZT attenuated diabetic nephropathy; however, AT exhibited greater efficacy desp

180 is (HR, 0.80; 95% CI, 0.77-0.82), membranous nephropathy (HR, 0.88; 95% CI, 0.83-0.93), membranoproli

181 y (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal se

182 , 0.32-2.52) but present in immunoglobulin A nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous n

183 ant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all other gr

184 patients with GN studied, patients with IgA nephropathy (IgAN) had the lowest mortality rates and pa

185 IgA nephropathy (IgAN) is a common chronic glomerular diseas

186 The role of immunosuppression in IgA nephropathy (IgAN) is controversial.

187 IgA nephropathy (IgAN) is the most common form of primary GN

188 IgA nephropathy (IgAN) is the most prevalent among primary g

189 IgA nephropathy (IgAN), characterized by mesangial IgA1 depo

190 ts with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN) (n=1

191 bout 6-8% of the disease heritability of IgA nephropathy (IgAN), suggesting that there are still a la

192 ay has a key role in the pathogenesis of IgA nephropathy (IgAN).

193 Most patients with idiopathic membranous nephropathy (IMN) have IgG4 autoantibodies against phosp

194 esigned to interfere with the development of nephropathy in a humanized mouse model of SCD.

195 de attenuates the manifestations of diabetic nephropathy in a type 1 diabetic animal model, OVE26.

196 inflammation and prevents the development of nephropathy in db/db mice.

197 ay be promising targets for the treatment of nephropathy in diabetes and obesity.

198 isms underlying the onset and progression of nephropathy in diabetic patients are not fully elucidate

199 heavy chain IIA are associated with diabetic nephropathy in European Americans and with sickle cell d

200 treated, prevented, and reversed established nephropathy in genetic models of diabetes.

201 examined the role of Nox5 in human diabetic nephropathy in human mesangial cells and in an inducible

202 ructive nature of vancomycin-associated cast nephropathy in mice, which we detected using different i

203 ration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diabetes.

204 sense mutations and has been associated with nephropathy in some carriers.

205 Sickle cell nephropathy is a common complication in patients with si

206 Diabetic nephropathy is a lethal complication of diabetes mellitu

207 Sickle cell disease (SCD)-associated nephropathy is a major source of morbidity and mortality

208 BK polyomavirus (BKV)-associated nephropathy is a threat to kidney allograft survival aff

209 Diabetic nephropathy is characterized by inflammation, fibrosis,

210 Finally, overt nephropathy is characterized by proteins involved in wou

211 material is minimized and the risk of acute nephropathy is reduced.

212 Cast nephropathy is the main cause of acute kidney injury in

213 BK virus (BKV)-associated nephropathy is the second leading cause of graft loss in

214 IgA nephropathy is thought to be associated with mucosal imm

215 the treatment regimen in type 2 diabetes and nephropathy is warranted.

216 II receptors (UTR) are increased in diabetic nephropathy, it remains unclear whether UII regulates GM

217 ts, and it may rarely cause JCPyV-associated nephropathy (JCPyVAN).

218 ibutes to the development of immune-mediated nephropathies like in lupus nephritis.

219 rade/class for disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and additiona

220 affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropathy.

221 lusion, the risk of radiocontrast-associated nephropathy may be overstated in the literature and over

222 , at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to reduc

223 mainstay for the treatment of minimal change nephropathy (MCN), which is characterised by an absence

224 pared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus nephritis,

225 rogate for long-term prognosis in membranous nephropathy (MGN), variability in proteinuria levels and

226 arget antigen identified in adult membranous nephropathy (MN) along with the major antigen phospholip

227 Primary membranous nephropathy (MN) is an autoimmune disease mainly caused

228 Membranous nephropathy (MN) is the most common cause of nephrotic s

229 two major autoantigens in primary membranous nephropathy (MN), and define two molecular subclasses of

230 for autoimmunity in patients with membranous nephropathy (MN).

231 tract (n = 637 [70.9%]), tubulointerstitial nephropathies (n = 92 [10.2%]), glomerulopathies (n = 69

232 biopsy specimens from patients with diabetic nephropathy (n = 9) and controls (n = 6).

233 Incident or worsening nephropathy occurred in 525 of 4124 patients (12.7%) in

234 ey disease (ARPKD) is an important childhood nephropathy, occurring 1 in 20,000 live births.

235 enal function loss in patients with diabetic nephropathy on chronic stable renin-angiotensin system i

236 In human and mouse type 2 diabetic nephropathy, only CD68(+) intrarenal monocytes expressed

237 nged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of deceased do

238 tic syndrome caused by idiopathic membranous nephropathy or focal segmental glomerulosclerosis were c

239 adults with CKD of unknown cause or familial nephropathy or hypertension.

240 or an association with severe retinopathy or nephropathy or their combination in the FinnDiane cohort

241 ia (OR, 4.52; CI, 2.33-8.77; P < 0.0001) and nephropathy (OR, 3.03; CI, 1.16-7.9; P = 0.02).

242 e, medullary cystic kidney disease, diabetic nephropathy, or CKD of unknown cause.

243 from patients with lupus nephritis, diabetic nephropathy, or nephrotic syndrome.

244 y have a significant favorable effect on IgA nephropathy outcomes.

245 ation: glomerulonephritis (P = 0.009), viral nephropathies (P = 0.002), interstitial fibrosis and tub

246 effects against the progression of diabetic nephropathy, partly by protecting podocytes.

247 The proportions of retinopathy, nephropathy, peripheral neuropathy, diabetic foot, and i

248 ed trials of rituximab in primary membranous nephropathy (PMN) have not been conducted.

249 ADCK4 nephropathy presented during adolescence (median age, 14

250 disease, inhibition of Jmjd3 and UTX abated nephropathy progression in mice with established glomeru

251 enal outcomes included incident or worsening nephropathy (progression to macroalbuminuria, doubling o

252 , during angiotensin II-induced hypertensive nephropathy provided novel insights into FSGS pathogenes

253 Polyomavirus-associated nephropathy (PVAN) after BK virus reactivation in kidney

254 Polyomavirus nephropathy (PVAN) is a common cause of kidney allograft

255 Polyomavirus-associated nephropathy (PVAN) occurs in a significant percentage of

256 Polyomavirus nephropathy (PVN) is a common viral infection of renal a

257 orrhagic cystitis and also with polyomavirus nephropathy (PVN).

258 ects with type 2 diabetes mellitus and overt nephropathy receiving angiotensin converting enzyme inhi

259 teinuria and glomerulosclerosis in radiation nephropathy remain largely unknown.

260 BK virus (BKV) nephropathy remains the main cause of renal graft loss a

261 98 patients with biopsy-proven myeloma cast nephropathy requiring hemodialysis treated at 48 French

262 g adolescence in ADCK4 than in WT1 and NPHS2 nephropathy, resulting in similar cumulative ESRD rates

263 Microvascular outcomes were nephropathy, retinopathy, and neuropathy.

264 Studies in patients with diabetic nephropathy showed a decrease in AIF within the renal tu

265 ression of Nox5 in a mouse model of diabetic nephropathy showed enhanced glomerular ROS production, a

266 f NADPH oxidase in animal models of diabetic nephropathy since Nox5 is absent in the mouse genome.

267 Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) Trial, 162 patients with IgAN an

268 ressive forms of nephrocalcinosis in oxalate nephropathy, such as primary hyperoxaluria.

269 entified in sows with porcine dermatitis and nephropathy syndrome (PDNS) and reproductive failure.

270 oductive failure, and porcine dermatitis and nephropathy syndrome (PDNS).

271 become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity upstre

272 s with or without treatment for presumed BKV nephropathy (tBKVN) using data from the United States Tr

273 with respect to annual eye examinations and nephropathy tests (P<0.001 for both comparisons); there

274 d a higher prevalence in recipients with BKV nephropathy than in those with viruria and viremia (P =

275 cted from beta-cell loss, hyperglycemia, and nephropathy that are present in ZDF littermates.

276 As a result, HIV-associated nephropathy, the classic HIV-driven kidney lesion among

277 In diabetic nephropathy, the gene expression of claudins, in particu

278 tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions of protein

279 al [95% CI], 1.05-1.31) for immunoglobulin A nephropathy to 2.09 (95% CI, 1.56-2.78) for membranoprol

280 otein interactions at each stage of diabetic nephropathy to provide an overview of the events underly

281 deposit formation in experimental membranous nephropathy to the role of a microRNA in FSGS.

282 Among patients with myeloma cast nephropathy treated with a bortezomib-based chemotherapy

283 g patients newly diagnosed with myeloma cast nephropathy treated with hemodialysis using a high-cutof

284 of the incidence of radiocontrast-associated nephropathy vary widely and suffer from misclassificatio

285 rotects kidneys against oxidative stress and nephropathy via stimulation of Sirtuin-1 expression and

286 atory burden or different etiology (diabetes nephropathy vs. other etiologies) of CKD could be associ

287 , although the incidence of contrast-induced nephropathy was higher in post-CABG patients (4.6% versu

288 elial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibition resto

289 ncing in a mouse model of folic acid-induced nephropathy, we identified ten genes that track kidney f

290 Rates of new or worsening nephropathy were lower in the semaglutide group, but rat

291 In incipient nephropathy, when albumin excretion rates are abnormal,

292 ly deficient in IL-17A developed more severe nephropathy, whereas administration of low-dose IL-17A p

293 renal cannabinoid-1 receptor (CB1R) induces nephropathy, whereas CB1R blockade improves kidney funct

294 n in a mouse model of unilateral obstructive nephropathy, which cannot be diagnosed with routine kidn

295 stitium in obstructive and aristolochic acid nephropathy, which correlates with progression of fibrot

296 ay hold promise in the treatment of diabetic nephropathy, which could eventually lead to applications

297 ovirus disease, herpes zoster, BK virus, and nephropathy, which led to the discontinuation of its dev

298 ed AS-IV to be beneficial to type 2 diabetic nephropathy, which might be associated with the inhibiti

299 ix affected individuals also had early-onset nephropathy with features of tubulo-interstitial nephrit

300 Dogs with X-linked hereditary nephropathy (XLHN) have a glomerular basement membrane d