{"title":"Changes in the glomerular pore size selectivity in patients with type II diabetes mellitus","authors":"Masatoshi Yamazaki, Nagayuki Tani, Kazumasa Igarashi, Hiroshi Nakamura, Takeshi Momotsu, Seiki Ito, Akira Shibata","doi":"10.1016/0891-6632(91)90047-S","DOIUrl":"10.1016/0891-6632(91)90047-S","url":null,"abstract":"<div><p>We measured the urinary excretion rate and clearance of three plasma proteins, albumin, transferrin, and IgG4, each of which has a similar isoelectric point, but a different molecular weight. This study consisted of 86 patients with type II diabetes mellitus and 15 healthy subjects. In the patients, the degree of the urinary excretion rate and clearance of both transferrin (TER and Ctrans) and IgG4 (IgG4 ER and CIgG4) closely correlated with that of the urinary excretion rate of albumin (AER). Although significant increases in the medians of TER and Ctrans were found even in the patients with AER of less than 5 μg/min, significant increases in the medians of IgG4 ER and CIgG4 were observed only in the patients with AER of more than 10 μg/min, in comparison with age-matched healthy subjects. Considering the biochemical properties of these proteins, our results indicate that an alteration in the glomerular size selectivity may appear even in patients with normoalbuminuria, and in patients with AER of more than 10 μg/min, more extensive damage in glomerular size selectivity may occur.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 138-139"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90047-S","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12932279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Renal metabolism of amino acids in early insulin-dependent diabetes mellitus","authors":"Giacomo Deferrari, Giacomo Garibotto , Cristina Robaudo , Stefano Saffioti , Roberto Pontremoli , Alberto Tizianello","doi":"10.1016/0891-6632(91)90033-L","DOIUrl":"10.1016/0891-6632(91)90033-L","url":null,"abstract":"<div><p>Renal metabolism of amino acids (AAs) was evaluated in 5 patients with early IDDM, and in 7 controls (C) in the basal state for 80 minutes after the ingestion of an AA mixture simulating an animal protein meal. Insulin was withdrawn 20 hours before the study. Renal metabolism of AAs was evaluated by the arterial-venous difference technique. In the basal state in IDDM, as in C, the kidney takes up large amounts of a few nonessential AAs (NEAAs): it releases many NEAAs and a few essential AAs (EAAs). After AA ingestion in C, renal extraction of most EAAs, mainly BCAAs, Lys, and Thr, occurs; Pro extraction also increases and a significant uptake of Gly, Glu, Asp, Orn, and Tyr takes place. EAA extraction accounts for 30–40% of total AA uptake. In IDDM, after AA ingestion, a) renal uptake of total AAs is significantly lower, owing mainly to a markedly lower uptake of BCAAs, Lys, and also of Pro, Orn, and Ala; b) renal EAA uptake accounts for less than 20% of total AA extraction. These results indicate that in IDDM postprandial renal N repletion is impaired and unbalanced.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 101-103"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90033-L","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12933023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial derangement: Possible initiator of microalbuminuria in NIDDM","authors":"Shigeo Takebayashi, Koji Kaneda","doi":"10.1016/0891-6632(91)90034-M","DOIUrl":"10.1016/0891-6632(91)90034-M","url":null,"abstract":"<div><p>Morphometric analysis of 80 renal biopsy specimens from patients with non-insulin-dependent diabetes mellitus, who had been classified into four groups by grade of proteinuria and renal function, revealed mitochondrial enlargement in the proximal tubules, with cellular hypertrophy as an initial morphologic change in the microalbuminuria. This was followed by a thickening of the proximal tubular basement membrane and an increased interstitial volume, causing persistent overt proteinuria. Glomerular nodular and sclerotic lesions and severe tubulointerstitial damage became evident in the advanced stages. As an initial cause of microalbuminuria, the mitochondrial abnormality disturbed adenosine triphosphate (ATP) metabolism in proximal tubules, reducing active transport and causing urinary excretion of low-molecular-weight protein.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 104-106"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90034-M","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12933024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Risk factors for retardation of renal function in IDDM and NIDDM with nephropathy","authors":"Shigeko Hara , Kenji Arizono , Yosifumi Ubara , Takasi Morita , Yosio Suzuki , Yousuke Ogura , Ryouko Hagura , Yasuo Akanuma","doi":"10.1016/0891-6632(91)90044-P","DOIUrl":"10.1016/0891-6632(91)90044-P","url":null,"abstract":"<div><p>Risk factors for retardation of renal function in 22 patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied and compared with those in 16 patients with insulin-dependent diabetes mellitus (IDDM). The annual decline rate of reciprocal serum creatinine was calculated from the rise of creatinine to the commencement of dialysis. The annual decline rate was compared with levels of blood pressure, fasting blood glucose, HbA<sub>1</sub>, and lipids, and clinical findings in patients with or without nephrotic syndrome during the same period. There was no significant difference in the rate of decline in levels of fasting blood glucose and HbA<sub>1</sub> in IDDM and NIDDM. In NIDDM, the major risk factor is hypertension, as in IDDM. Triglycerides and total cholesterol also play roles in the retardation of renal function. Nephrotic syndrome also influenced the retardation of renal function in both IDDM and NIDDM.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 131-133"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90044-P","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12933680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Natural history and pathogenesis of diabetic nephropathy","authors":"GianCarlo Viberti , James D. Walker","doi":"10.1016/0891-6632(91)90022-H","DOIUrl":"10.1016/0891-6632(91)90022-H","url":null,"abstract":"","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 72-75"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90022-H","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12934010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Robert G. Nelson , William C. Knowler , Peter H. Bennett
{"title":"Natural history of diabetic nephropathy in non-insulin-dependent diabetes mellitus","authors":"Robert G. Nelson , William C. Knowler , Peter H. Bennett","doi":"10.1016/0891-6632(91)90023-I","DOIUrl":"10.1016/0891-6632(91)90023-I","url":null,"abstract":"","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 76-78"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90023-I","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12934015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Liliane J. Striker, Toshio Doi, Francesco Conti, Gary E. Striker
{"title":"Role of mesangial cells in glomerulosclerosis","authors":"Liliane J. Striker, Toshio Doi, Francesco Conti, Gary E. Striker","doi":"10.1016/0891-6632(91)90018-K","DOIUrl":"10.1016/0891-6632(91)90018-K","url":null,"abstract":"","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 60-61"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90018-K","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12828638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L.B. Zimmerhackl , S. Pfleiderer , R. Kinne , F. Manz , G. Schuler , M. Brandis
{"title":"Tamm-Horsfall-Protein excretion as a marker of ascending limb transport indicates early renal tubular damage in diabetes mellitus type I","authors":"L.B. Zimmerhackl , S. Pfleiderer , R. Kinne , F. Manz , G. Schuler , M. Brandis","doi":"10.1016/0891-6632(91)90037-P","DOIUrl":"10.1016/0891-6632(91)90037-P","url":null,"abstract":"<div><p>Tamm-Horsfall Protein (THP) is a 95 kD glycoprotein which is secreted in the thick ascending loop of Henle (TALH) of the kidney. After renal tubular damage the secretion of THP is reduced. In diabetes mellitus (DM), TALH has not been studied. To differentiate between glomerular (albumin), proximal tubular microglobulinuria (<em>α</em><sub>1</sub>-microglobulin), and TALH function (THP), we investigated 65 patients 4–61 years of age. In well-controlled DM, mean hemoglobin A<sub>1</sub> equalled 7.4% and proximal tubular parameters indicated reversible damage early after onset. THP excretion (per 24 hrs or per day) was significantly elevated in DM duration of greater than ten years, suggesting enhanced TALH ion transport (glomerular hyperfiltration). THP secretion decreased in DM duration of greater than 15 years despite normal albumin excretion. Thus, renal THP excretion indicates early medullary dysfunction (TALH) in DM type I.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 112-114"},"PeriodicalIF":0.0,"publicationDate":"1991-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90037-P","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12886486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P.G. Newrick , C. Bowman , D. Green , I.A.D. O'Brien , S.R. Porter , C. Scully , R.J.M. Corrall
{"title":"Parotid salivary secretion in diabetic autonomic neuropathy","authors":"P.G. Newrick , C. Bowman , D. Green , I.A.D. O'Brien , S.R. Porter , C. Scully , R.J.M. Corrall","doi":"10.1016/0891-6632(91)90008-D","DOIUrl":"10.1016/0891-6632(91)90008-D","url":null,"abstract":"<div><p>Parotid salivary flow rates and amylase concentrations were measured in three groups of eight subjects each (normal control, non-neuropathic diabetic, and neuropathic diabetic). Flow rates were significantly reduced in neuropathic diabetic patients as compared with normal controls (<em>p</em> < 0.001) and non-neuropathic diabetic patients (<em>p</em> < 0.02). Amylase concentrations were similar. These data are consistent with parasympathetic denervation of the parotid gland in diabetic neuropathy and provide evidence for a widespread distribution of autonomic denervation in diabetes.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 1","pages":"Pages 35-37"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90008-D","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12877269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Albuminuria and associated medical risk factors: A cross-sectional study in 476 type I (insulin-dependent) diabetic patients. Part 1","authors":"O. Torffvit , E. Agardh , C-D. Agardh","doi":"10.1016/0891-6632(91)90006-B","DOIUrl":"10.1016/0891-6632(91)90006-B","url":null,"abstract":"<div><p>Albumin concentration in a morning urine sample was analyzed in a cross-sectional study in 476 insulin-dependent diabetic patients. The following groups of patients were defined: A) normal urinary albumin (urine albumin <12.5 mg/L); B) high normal albuminuria (12.5–30 mg/L); C) microalbuminuria, ie, incipient nephropathy (31–299 mg/L); and D) clinical nephropathy (≥300 mg/L). The prevalences of incipient and clinical diabetic nephropathy were 24.8 and 14.4%, respectively. There were no differences in clinical parameters such as age, age at onset or duration of diabetes, blood pressure, serum creatinine, or HbA<sub>1c</sub> levels between groups A and B. The frequency of retinopathy in these groups was 55 and 50%, respectively. In group C, there were increases in age, duration of diabetes, blood pressure, serum creatinine, and HbA<sub>1c</sub> levels. The frequency of retinopathy was higher (80%), and more patients had severe forms (47%). In group D, there were further increases in all parameters and, in addition, younger age at onset of diabetes. The frequency of retinopathy was 97%, and severe forms of retinopathy were more common (86%). Seventeen percent of the patients were treated for hypertension. These patients were older, had longer duration of diabetes, and had higher levels of blood pressure, serum creatinine, and urinary albumin, as well as a younger age at onset of diabetes than patients not requiring antihypertensive treatment.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 1","pages":"Pages 23-28"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0891-6632(91)90006-B","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12991915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}