Hiroshi Kida, Mituhiro Yoshimura, Kenzo Ikeda, Yafumi Saitou, Yutaka Noto
{"title":"Pathogenesis of diabetic nephropathy in non-insulin-dependent diabetes mellitus","authors":"Hiroshi Kida, Mituhiro Yoshimura, Kenzo Ikeda, Yafumi Saitou, Yutaka Noto","doi":"10.1016/0891-6632(91)90025-K","DOIUrl":"10.1016/0891-6632(91)90025-K","url":null,"abstract":"<div><p>To elucidate the characteristics of diabetic nodular lesions and the process of progression of diabetic glomerulosclerosis, kidney specimens obtained from 185 patients with non-insulin-dependent diabetes mellitus (NIDDM) were observed using light, electron, and immunofluorescence microscopes. The results suggest the following. First, there are two distinct subtypes of nodular lesions: One is formed by the progression and expansion of diffuse lesions; the other, showing a concentrically layered structure, is probably formed in the process of reconstruction of mesangiolysis. Second, there are three phases in the process of progression of diabetic glomerulosclerosis: In the first phase, arteriolosclerosis and diffuse lesions appear; in the second phase, mesangiolysis and nodular lesions develop in association with moderately advanced arteriolosclerosis; and in the third phase, exudative lesions and hyalinized glomeruli appear in association with advanced arteriolosclerosis together with advanced interstitial lesions. In the progression of the phases and in the development of mesangiolysis and layered nodular lesions, disturbed blood flow into glomeruli in consequence of diabetic arteriolosclerosis could be essential.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 82-83"},"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)90025-K","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12934013","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":"Comparison of renal hemodynamics in early non-insulin-dependent and insulin-dependent diabetes mellitus","authors":"Kazufumi Ishida, Fukashi Ishibashi, Seiryo Takashina","doi":"10.1016/0891-6632(91)90049-U","DOIUrl":"10.1016/0891-6632(91)90049-U","url":null,"abstract":"<div><p>The differences in deranged renal hemodynamics in non-insulin-dependent diabetes mellitus (NIDDM) and insulin-dependent diabetes mellitus (IDDM) have never been fully investigated. Whether or not autoregulatory mechanism of renal hemodynamics in NIDDM and IDDM is preserved remains to be clarified.</p><p>In the present study we directly compared renal hemodynamics and its autoregulatory function in the early stage of NIDDM and IDDM before and after short-term glycemic control. Before glycemic control, mildly exaggerated glomerular filtration rate (GFR), subnormal renal plasma flow (RPF), and elevated filtration fraction (FF) were found in NIDDM as well as in IDDM; but there were no differences in these parameters of renal hemodynamics between the two types of diabetics. Glycemic control decreased GFR, whereas it did not alter RPF, resulting in normalization of FF in NIDDM and in IDDM. Before glycemic control, mean blood pressure was significantly correlated with GFR, but was not correlated after glycemic control in either type of diabetes. In conclusion, hyperglycemia induced glomerular hyperfiltration evenly and disturbed autoregulation of renal hemodynamics in NIDDM and in IDDM.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 143-145"},"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)90049-U","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12932281","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}
S. Haisa , T. Norii , E. Takatori , A. Goto , S. Morioka , K. Uchida , H. Himei
{"title":"Effects of angiotensin-converting enzyme inhibitor (alacepril) and calcium antagonist (nicardipine) in hypertensive non-insulin-dependent diabetic patients with microalbuminuria","authors":"S. Haisa , T. Norii , E. Takatori , A. Goto , S. Morioka , K. Uchida , H. Himei","doi":"10.1016/0891-6632(91)90058-W","DOIUrl":"10.1016/0891-6632(91)90058-W","url":null,"abstract":"<div><p>The influence of alacepril (50 mg/day) on arterial blood pressure and microproteinuria in 26 hypertensive non-insulin-dependent diabetic patients was studied for 16 weeks. Alacepril reduced blood pressure gradually from <span><math><mtext>175</mtext><mtext>88</mtext></math></span> (standard error of mean [SEM] <span><math><mtext>2.6</mtext><mtext>1.7</mtext></math></span>) to <span><math><mtext>152</mtext><mtext>81</mtext></math></span> (<span><math><mtext>3.3</mtext><mtext>2.0</mtext></math></span>) mm Hg (<em>P</em> < .005) and albuminuria from 160.6 (SEM 29.1) to 98.1 (14.1) mg/g Cr (<em>P</em> < .05), while serum blood urea nitrogen, creatinine, HbA<sub>1c</sub>, and fructosamine (FRA) remained stable. No significant changes occurred in the urinary β<sub>2</sub> microglobulin and <em>N</em>-acetyl-β-<span>d</span>-glucosaminidase levels. As compared with the effects of a calcium antagonist (nicardipine, 60 mg/day) that reduced blood pressure from <span><math><mtext>170</mtext><mtext>92</mtext></math></span> (SEM <span><math><mtext>2.5</mtext><mtext>1.4</mtext></math></span>) to <span><math><mtext>154</mtext><mtext>84</mtext></math></span> (<span><math><mtext>2.5</mtext><mtext>1.5</mtext></math></span>) mm Hg (<em>P</em> < .001) and albuminuria from 162.2 (SEM 33.9) to 95.4 (25.0) mg/g Cr (not significant), it is suggested that the angiotensin-converting enzyme inhibitor (alacepril) may have an advantageous renal effect in spite of its mild antihypertensive effect.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 162-164"},"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)90058-W","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12932286","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}
S. Okamoto, M. Ikeda, T. Morise, I. Miyamori, R. Takeda
{"title":"Elevated endogenous Na-K-ATPase inhibitor activity in hypertensive diabetic patients with a family history of hypertension","authors":"S. Okamoto, M. Ikeda, T. Morise, I. Miyamori, R. Takeda","doi":"10.1016/0891-6632(91)90050-Y","DOIUrl":"10.1016/0891-6632(91)90050-Y","url":null,"abstract":"<div><p>Digitalis-like substance (DLS) was measured by Na-K-ATPase inhibitor (ATPI) activity and digitalis-like immunoreactivity (DLI) in 100 patients with type II diabetes. Hypertensive diabetic patients with a positive family history for hypertension had high ATPI levels compared with those patients with a negative family history for the disease. DLI level did not differ between groups. There was no significant difference in ATPI and DLI levels among three groups based on level of urinary albumin excretion. These data suggest that a circulating factor (or circulating factors) determined by ATPI may be linked with genetic factors in the development of hypertension, but not to the development of diabetic nephropathy.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 146-147"},"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)90050-Y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12828637","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":"Three-dimensional architecture of glomerular extracellular matrices in diabetic glomerulosclerosis","authors":"Hirofumi Makino, Shigeaki Nishimura, Toshinori Haramoto, Yasushi Yamasaki, Shuji Ikeda, Zensuke Ota","doi":"10.1016/0891-6632(91)90041-M","DOIUrl":"10.1016/0891-6632(91)90041-M","url":null,"abstract":"<div><p>The three-dimensional ultrastructural changes of the glomerular extracellular matrices in diabetic glomerulosclerosis were studied in acellular rat and human diabetic glomeruli by scanning electron microscopy. The mesangial matrix appeared as fenestrated septa with oval stomata between the glomerular capillaries in normal control specimens. In diabetic glomerulosclerosis, both in humans and rats, expansion of mesangial matrix and narrowing of the mesangial fenestrae were observed. A thin layer of the mesangial matrix extended into the peripheral glomerular basement membrane (GBM) subendothelially. Thickening of the GBM in diabetic nephropathy might be due to expansion of the mesangial matrix into the peripheral GBM.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 124-125"},"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)90041-M","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12933677","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":"Glucose-induced production of type IV collagen and laminin P1 from cultured human umbilical vein endothelial cells","authors":"Shigeki Moritani , Kiyohiko Negishi , Toshiro Watanabe , Shunichiro Shunto , Naoki Serizawa , Masao Suzuki , Masaki Takahashi , Shigehiro Katayama , Jun Ishii , Shoji Kawazu","doi":"10.1016/0891-6632(91)90075-Z","DOIUrl":"10.1016/0891-6632(91)90075-Z","url":null,"abstract":"<div><p>To study the effect of high glucose on the production of type IV collagen and laminin P1 from the cultured human umbilical vein endothelial cells (HUVEC), we measured type N collagen and laminin P1 from HUVEC that were cultured under different conditions. The concentrations of type IV collagen in the cultured medium for high glucose (30 mM <span>d</span>-glucose), <span>l</span>-glucose (30 mM), or mannitol (30 mM). The increase of type IV collagen was dependent on the glucose concentration in the medium. The contents of type IV collagen in the cultured cells were also increased in high-glucose incubation compared with low glucose or <span>l</span>-glucose incubation. In contrast, the levels of laminin P1 in the medium cultured with high glucose were similar to those with low glucose or <span>l</span>-glucose. These results suggest that the increased production of type IV collagen may contribute to the thickening of basement membranes and may be linked to the development of diabetic nephropathy.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 201-203"},"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)90075-Z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12934003","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":"Clinical significance of microalbuminuria in Japanese subjects with non-insulin-dependent diabetes","authors":"Yukio Shigeta, Masakazu Haneda, Ryuichi Kikkawa","doi":"10.1016/0891-6632(91)90026-L","DOIUrl":"10.1016/0891-6632(91)90026-L","url":null,"abstract":"<div><p>In order to elucidate the clinical significance of microalbuminuria in non-insulin-dependent diabetes mellitus (NIDDM), 62 Japanese subjects with NIDDM and without proteinuria were followed for three years. After the three-year follow up, four (19%) of 21 microalbuminuric patients—albumin excretion rates (AER) greater than 15 μg/min—developed overt proteinuria, while none of the 42 normoalbuminuric patients did. Among these normoalbuminuric patients, eight patients (19.5%) developed microalbuminuria. The microalbuminuric patients who developed overt proteinuria had higher AER at the beginning of the study than the patients who stayed microalbuminuric. The patients who developed microalbuminuria showed a significantly higher systolic blood pressure in the final year than the patients who stayed normoalbuminuric. These results indicate that microalbuminuria precedes overt proteinuria in Japanese NIDDM, and progression of diabetic nephropathy is rapid and associated with a rise in blood pressure.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 84-86"},"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)90026-L","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12934014","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":"Serum or urinary concentration of type IV collagen in diabetics","authors":"Toshiro Watanabe , Kiyohiko Negishi , Shigehiro Katayama , Jun Ishii , Shoji Kawazu","doi":"10.1016/0891-6632(91)90070-6","DOIUrl":"10.1016/0891-6632(91)90070-6","url":null,"abstract":"<div><p>Concentrations of serum or urinary type IV collagen, determined by sandwich enzyme immunoassay, were significantly elevated in diabetics compared to controls (<em>P</em><.01). Serum or urinary levels of type IV collagen were significantly increased in patients with microangiopathy compared to those without microvascular disease (<em>P</em> < .05). Serum type IV collagen levels were also augmented in diabetics who showed an increased albumin index for 1 year. Serum levels of type IV collagen were not affected by any conditions of metabolic control.</p><p>The measurement of serum or urinary type IV collagen may be a useful indicator for monitoring the development of diabetic microangiopathy, especially in early diabetic nephropathy.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 191-192"},"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)90070-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12932703","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":"Asymptomatic ischemic heart disease and diabetic nephropathy: Relationship between prevalence of asymptomatic ischemic heart disease and urinary albumin excretion rate","authors":"Nagayuki Tani , Asako Hiroshima , Yutaka Kobayashi , Kazumasa Igarashi , Masatoshi Yamazaki , Hiroshi Nakamura , Asao Nakazawa , Seiki Ito , Akira Shibata","doi":"10.1016/0891-6632(91)90061-S","DOIUrl":"10.1016/0891-6632(91)90061-S","url":null,"abstract":"<div><p>To examine whether prevalences of asymptomatic ischemic heart diseases in type II diabetic patients are correlated with the degree of diabetic nephropathy, <sup>201</sup>Tl scintigraphies with dipyridamole loading were performed in 28 type II diabetic patients without any chest discomforts. Positive findings of ischemic changes were found in 5 (28%) of 18 patients with normoalbuminuria (urinary albumin excretion rate, AER < 20 μg/min) and 5 (50%) of 10 patients with micro- or macroalbuminuria (AER > 20 μg/min). Coronary angiography (CAG) was performed in 6 of 10 patients with positive findings of <sup>201</sup>Tl scintigraphy. No stenotic findings were found in any patients, but wall motion was decreased in some patients and pulmonary artery pressure was increased in one patient. As stenosis of arteries with diameter of more than 0.3 mm can be detected by CAG, it seems likely that microangiopathy may play some role in the pathogenesis of asymptomatic ischemic heart disease detected with <sup>201</sup>Tl scintigraphy.</p></div>","PeriodicalId":77636,"journal":{"name":"The Journal of diabetic complications","volume":"5 2","pages":"Pages 169-170"},"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)90061-S","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12932181","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}