Non-diabetic Nephropathy Patients Research Articles

Age at onset of type 1 diabetes between puberty and 30 years old is associated with increased diabetic nephropathy risk

Diabetic nephropathy is a critical complication of patients with type 1 diabetes, while epidemiological studies were scarce among Asian countries. We conducted a cross-sectional study to identify factors associated with diabetic nephropathy by questionnaires, using student’s t-test, chi-square test, and multivariable logistic regression. Among 898 participants, 16.7% had diabetic nephropathy. Compared with non-diabetic nephropathy patients, the patients with diabetic nephropathy had significantly higher percentage with onset age of type 1 diabetes between puberty and under 30 years old (female ≥ 12 or male ≥ 13 years old to 29 years old), longer diabetes duration, having family history of diabetes and diabetic nephropathy, accompanied with hypertension, hyperlipidemia, or coronary artery disease (CAD). Compared with patients with onset age before puberty, the odds of diabetic nephropathy occurrence increased to 1.61 times in patients with onset age between puberty and under 30 years old (p = 0.012) after adjusting diabetes duration. Age of diabetes onset between puberty and under 30 years old, diabetes duration, HbA1c, hospital admission within 3 years, diabetic retinopathy, hypertension, systolic blood pressure (SBP), triglyceride levels, and use of angiotensin converting enzyme inhibitor (ACEI) and/or angiotensin receptor blockers (ARB) were independent factors associated with diabetic nephropathy Screening for proteinuria is important in daily clinical practice and should be part of diabetes self-management education for patients with type 1 diabetes.

Different time points, different blood pressures: complexity of blood pressure measurement in hemodialysis patients.

We used our established database to investigate predialysis blood pressure (BP) measurements at different time points. Our study period spanned from 1 January 2019 to 31 December 2019. The different time points included: the long interdialytic interval versus the short interdialytic interval; different hemodialysis shifts. Multiple linear regression was used to explore the association between BP measurements and different time points. A total of 37 081 cases of hemodialysis therapies were included. After a long interdialytic interval, predialysis SBP and DBP were significantly elevated. Predialysis BP was 147.72/86.73 mmHg on Monday and 148.26/86.52 mmHg on Tuesday, respectively. Both predialysis SBP and DBP were higher in the a.m. shift. The mean BP in the a.m. and p.m. shifts were 147.56/87 mmHg and 144.83/84.64 mmHg, respectively. In both diabetic nephropathy and non-diabetic nephropathy patients, higher SBP measurements after a long interdialytic interval were observed; however, in diabetic nephropathy patients, we did not find significant differences in DBP among different dates. In diabetic nephropathy and non-diabetic nephropathy patients, we observed that the effect of different shifts on BP was similar. In Monday, Wednesday and Friday subgroups, the long interdialytic interval was also associated with BP; however, in Tuesday, Thursday and Saturday subgroups, different shifts but not the long interdialytic interval was associated with BP. The long interdialytic interval and different hemodialysis shifts have a significant effect on predialysis BP in patients with hemodialysis. When interpreting BP in patients with hemodialysis, different time points is a confounder.

The efficacy and safety of SGLT2 inhibitors in patients with non-diabetic chronic kidney disease: a systematic review and meta-analysis.

In recent years, increasing evidence has shown that sodium-glucose cotransporter 2 inhibitors (SGLT2i) drugs have potential renoprotective effects in patients with diabetes mellitus (DM). However, the renal protective effect of SGLT2i in non-diabetic nephropathy patients has not been extensively demonstrated. In this systematic review and meta-analysis, we aimed to evaluate the renal protective effect and safety of SGLT2i in non-diabetic nephropathy patients. we searched for relevant clinically randomised controlled trials and analyzed the effects of SGLT2i on estimated glomerular filtration rate (eGFR), urinary albumin/creatinine ratio (UACR), and systolic blood pressure (SBP) and the incidence of adverse events in patients with non-diabetic nephropathy. We collated and analysed clinical data from six groups of patients with nondiabetic nephropathy. It was found that the SGLT2i significantly delayed the decline in eGFR [MD = 1.35ml/min/1.73 m2, 95% CI 0.84, 1.86), P < 0.0001]. Furthermore, the SGLT2i significantly reduced UACR [MD = - 24.47% l, 95% CI (- 38.9, -10.04), P = 0.0009], and showed a greater decrease in SBP [MD = - 4.13mmHg, 95% CI (-7.49, - 0.77), P = 0.02]. There was no significant difference in the incidence of adverse reactions between dapagliflozin/empagliflozin and the control group [OR = 1.14, 95% CI (0.88, 1.47), P = 0.33]. This study shows that SGLT2i help to delay the progression of non-diabetic kidney disease. Therefore, SGLT2i may contribute to the general treatment of nondiabetic nephropathy.

MO631: Diabetic Retinopathy and/or Diabetic Nephropathy Confers A Worse Renal Prognosis

Abstract BACKGROUND AND AIMS Around 50%–60% lesions of non-diabetic nephropathy (NDN) have been identified in patients with diabetes and renal biopsy. NDN patients have a better renal prognosis and survival. Diabetic retinopathy (DR) is a microvascular complication of diabetes frequently associated with diabetic nephropathy (DN). The objective of the work is to study the renal prognosis and survival of patients with DN with or without DR. METHOD Retrospective, observational, multicenter study of the pathological results of diabetic patients with renal biopsy was undertaken. A total of 18 Spanish centers have participated. RESULTS Cohort of 832 patients: 621 men (74.6%), median age 61.7 ± 12.8 years, median creatinine 2.8 ± 2.2 mg/dL and proteinuria 2.7 (1.2–5.4) g/24 h. Of them, 26.6% (n = 221) presented DR, 18.8% (n = 156) peripheral vasculopathy and 17.7% (n = 147) ischemic heart disease. On biopsy, 39.5% (n = 329) of patients had DN, 413 (49.6%) NDN and 90 (10.8%) mixed forms. We evidenced more DR in the DN group compared with the other two groups (44.1% versus 11.1% in NDN and 33.3% in mixed forms). Regarding renal prognosis, 58.9% (n = 109) of patients with DR and DN and mixed forms required RRT versus 40.7% (n = 88) of patients without DR. A total of 39.1% (n = 18) of patients with DR and NDN required renal replacement therapy (RRT) versus 23.9% (n = 79) of patients without DR. Regarding mortality, 28.6% (n = 50) of patients with DR and DN or mixed forms died during the follow-up versus 22.7% (n = 49) of patients without DR. A total of 15.2% (n = 7) of patients with DR and NDN died and 15.4% (n = 51) of patients without DR. In survival analysis (Kaplan—Meier curves), patients with DR had worse renal prognosis (P &amp;lt; 0.001), patients with DN (P &amp;lt; 0.001) and patients with DR and/or DN and mixed forms (P = 0.02). Cox regression analysis identified as independent risk factors of RRT: age (OR 1.014;1.025–1.004, P = 0.006), creatinine (OR 1.262; 1.217–1.309; P &amp;lt; 0.001), proteinuria (OR 1.057; 1.03–1.085; P &amp;lt; 0.001), DR (OR 1.359; 1.007–1.833; P = 0.045), DR and/or DN (OR 1.59; 2.42–1.04; P = 0.033) and DN (OR1.489; 1.05–2.11; P = 0.026). CONCLUSION The presence of DR and/or DN confers a worse renal prognosis. The diagnosis of diabetic microangiopathy in terms of retinopathy and/or diabetic nephropathy is crucial since it confers a worse renal prognosis indicating patients at risk of progression to end-stage renal disease.

Differences between diabetic and non-diabetic nephropathy patients in cardiac structure and function at the beginning of hemodialysis and their impact on the prediction of mortality.

ObjectivesTo characterize differences in cardiac structure and function in hemodialysis (HD) patients with diabetic nephropathy (DN) and in those without using echocardiography and to determine their impact on the prediction of mortality using echocardiographic parameters.MethodsClinical, laboratory, and echocardiographic data were collected from patients commencing HD.ResultsCompared with those without DN, patients with DN had lower peak velocity of the early diastolic wave (e′), larger left atria, and higher peak early diastolic velocity (E)/e′ and peak velocity of tricuspid regurgitation (TR). In addition, a larger proportion of DN patients had a combination of left ventricular (LV) diastolic dysfunction, cardiac valve calcification, moderate-to-severe cardiac valve regurgitation (CVR), and at least moderate pericardial effusion (PE). After accounting for age, sex, smoking, hypertension, hemoglobin, and albumin, DN was responsible for e′ < 10 cm/s, E/e′ >13 m/s, TR >2.8 m/s, LV diastolic dysfunction, CVR, and PE. LV diastolic dysfunction and E/e′ >13 were the most useful predictors of mortality in patients with DN.ConclusionsPatients with DN who undergo HD tend to have worse LV diastolic function and are more likely to have heart valve problems. LV diastolic dysfunction and E/e′ are predictors of death in DN patients.

DIFFERENCES IN INTERLEUKIN 18 LEVELS IN DIABETIC NEPHROPATHY AND NON-DIABETIC NEPHROPATHY PATIENTS

Background: Diabetic nephropathy is a common complication in diabetics. In this disease damage to the kidney filter or known as glomerulus. Therefore causing glomerular damage, the amount of blood protein is excreted into the urine abnormally. IL-18 is a proinflammatory cytokine produced from activated macrophages, serum IL-18 levels are produced to increase in patients with diabetic nephropathy. IL-18 which affects the production of other proinflammatory cytokines, endothelial apoptosis, ICAM-1 certification enhancement. Thus, IL-18 may be an important factor not only in the process of atherosclerosis but also in the development of diabetic nephropathy. Aim: Knowing the IL-18 levels in diabetic nephropathy and non-diabetic nephropathy patients. Methods: The study was conducted using the Cross Section method. This study took blood samples from 60 diabetic patients, of which 30 patients with nephropathy and 30 patients with type 2 diabetes. Then took 5 ml of blood from a vein and assessed serum IL-18 levels in all patients. Results: The study was conducted for 3 months, 41 men (68.3%) 19 women (37.1%). Serum IL-18 levels were significantly increased in patients with diabetic nephropathy compared with patients with type 2 diabetes (362.7 vs 55.7 pg / ml, p &lt;0.001) Conclusions: Increased IL-18 levels in diabetic nephropathy patients can be used as prognostic events for diabetic nephropathy.

Comparative analysis of diabetic nephropathy and non-diabetic nephropathy disease.

ObjectiveClinical symptoms of diabetic nephropathy patients and non-diabetic nephropathy are compared and analyzed, hemodialysis effect and quality of life of two kinds of nephrotic patients are analyzed.MethodsRespectively extract 1300 cases of diabetic nephropathy and non-diabetic nephropathy patients admitted to different hospitals during December 2011-December 2014. Based on whether the patient suffers from diabetes, they were divided into diabetic group and control group. Hemodialysis of two groups of patients were followed up to observe effectiveness of blood treatment, and complications were observed after one year of follow-up.ResultsHematodialysis effectiveness of diabetic nephropathy patients is significantly lower than that of non-diabetic nephropathy group. After 1 year’s follow-up, it can be found that survival rate of diabetic nephropathy patients is much lower than that of control group. In statistical comparison of data involved in the two groups of patients, P < 0.05, the difference is statistically significant.ConclusionTreatment effect of diabetic nephropathy patients is relatively poor compared to that of non-diabetic patients. In clinics, management and prevention of diabetic patients should be strengthened to avoid complication of nephropathy which brings serious injury to patients.

Urinary Excretion of Kidney Aquaporins as Possible Biomarker of Diabetic Nephropathy

BackgroundDiabetic nephropathy (DN) is is classified into four hierarchical glomerular lesions on the basis of histological analysis of kidney biopsies. This is clearly a highly invasive diagnostic approach numerous studies have been conducted to identify a non‐invasive biomarker of the disease, but none of these is considered to be sufficiently specific and sensitive Experimental evidences showed that the water channel aquaporins (AQP), expressed at the plasma membrane of epithelial cells lining in the kidney tubule, are often dysregulated during DN. Interestingly, apical membrane protein are excreted in the urinary space as nano‐scale exosome vesicles, to an extent proportional to their amount expressed at the plasma membrane, thus allowing their quantitation in urine samples.MethodsIn this work we compared excretion of AQP5 and AQP2 (uAQP5 and uAQP2) in the urine of 35 diabetic patients: 12 with histological diagnosis of DN, 12 with with normal renal function and normoalbuminuric (DM) and 11 with non‐diabetic nephropathy (NDN). Both proteins were quantified by ELISA method on urine samples and the results were validated by Western blotting analysis on the exosome fraction isolated by ultracentrifugation.ResultsBothELISA and Western blotting analysis independently showed that uAQP5 was three‐ to fourfold higher in DN patients (7458 ± 2576, p &lt;0.05) compared to the other two groups (D 847,2 ± 70,51; NDN1882 ± 215). uAQP5 was not statistically different between D and NDN patients. Strikingly, uAQP5 dramatically increased in parallel with the clinical severity of DN. The same analysis showed comparable results for uAQP2.ConclusionsOur data showed, for the first time, that uAQP5 and uAQP2 dramatically and specifically increase in patients with DN and positively correlate with the histological class of DN. Taken together these data suggest a possible role of AQP5 and AQP2 as novel non‐invasive biomarkers to help diagnosing DN and classifying its histological stage.Support or Funding InformationNon U.S.

Renal Replacement Therapy: Purifying Efficiency of Automated Peritoneal Dialysis in Diabetic versus Non-Diabetic Patients.

Background: In order to reduce the cardiovascular risk, morbidity and mortality of peritoneal dialysis (PD), a minimal level of small-solute clearances as well as a sodium and water balance are needed. The peritoneal dialysis solutions used in combination have reduced the complications and allow for a long-time function of the peritoneal membrane, and the preservation of residual renal function (RRF) in patients on peritoneal dialysis (PD) is crucial for the maintenance of life quality and long-term survival. This retrospective cohort study reviews our experience in automatic peritoneal dialysis (APD) patients, with end-stage renal disease (ESRD) secondary to diabetic nephropathy (DN) in comparison to non-diabetic nephropathy (NDN), using different PD solutions in combination. Design: Fifty-two patients, 29 diabetic and 23 non-diabetic, were included. The follow-up period was 24 months, thus serving as their own control. Results: The fraction of renal urea clearance (Kt) relative to distribution volume (V) (or total body water) (Kt/V), or creatinine clearance relative to the total Kt/V or creatinine clearance (CrCl) decreases according to loss of RRF. The loss of the slope of RRF is more pronounced in DN than in NDN patients, especially at baseline time interval to 12 months (loss of 0.29 mL/month vs. 0.13 mL/month, respectively), and is attenuated in the range from 12 to 24 months (loss of 0.13 mL/month vs. 0.09 mL/month, respectively). Diabetic patients also experienced a greater decrease in urine output compared to non-diabetic, starting from a higher baseline urine output. The net water balance was adequate in both groups during the follow up period. Regarding the balance sodium, no inter-group differences in sodium excretion over follow up period was observed. In addition, the removal of sodium in the urine output decreases with loss of renal function. The average concentration of glucose increase in the cycler in both groups (DN: baseline 1.44 ± 0.22, 12 months 1.63 ± 0.39, 24 months 1.73 ± 0.47; NDN: baseline 1.59 ± 0.40, 12 months 1.76 ± 0.47, 24 months 1.80 ± 0.46), in order to maintain the net water balance. The daytime dwell contribution, the fraction of day and the renal fraction of studies parameters provide sustained benefit in the follow-up time, above 30%. Conclusions: The wet day and residual renal function are determinants in the achievement of the objective dose of dialysis, as well as in the water and sodium balance. The cause of chronic kidney disease (CKD) does not seem to influence the cleansing effectiveness of the technique.

Efficacy of urinary N-acetyl-β-D-glucosaminidase to evaluate early renal tubular damage as a consequence of type 2 diabetes mellitus: a cross-sectional study

We assessed the prognostic accuracy of urinary N-acetyl-β-D-glucosaminidase (NAG), an early proximal tubular damage marker for the onset of diabetic nephropathy. The study included 491 eligible participants with 76 healthy controls, 194 type 2 diabetes mellitus (T2DM) patients with 0–5, 5–10, 10–15, and 15–20 years of T2DM duration, 71 microalbuminuric patients, 100 diabetic nephropathy patients, and 50 non-diabetic nephropathy patients. Fasting glucose, serum fructosamine, HbA1C, urinary microalbumin, serum creatinine, estimated glomerular filtration rate (eGFR), serum NAG, and urinary NAG were estimated. We compared urinary NAG activity with other well-established markers of diabetic nephropathy like microalbuminuria, eGFR, and serum creatinine. Urinary NAG excretion was increased by 8 and 12 folds in T2DM patients of 10–15 and 15–20 years of diabetes duration (p < 0.0001), respectively, without the appearance of microalbuminuria. The urinary NAG activity increased 16 and 18 fold in moderately increased albuminuria and diabetic nephropathy patients, respectively (p < 0.0001), without any change in non-diabetic nephropathy patients. A cutoff value of 3 U/L of urinary NAG has demonstrated a sensitivity of 96.1 % and a specificity of 100 % discriminating healthy controls from patients with T2DM duration of 10–15 years (AUC 1.000) and 15–20 years (AUC 0.999); microalbuminuria (AUC 0.999), and diabetic nephropathy (AUC 1.000). Urinary NAG excretion gradually increases with the increase in duration of diabetes and appeared much before the microalbuminuria, decreased eGFR, and increased serum creatinine. Thus, the urinary NAG may be considered as a potential site-specific early tubular damage marker leading to diabetic nephropathy.

Japanese society for dialysis therapy clinical guideline for "hemodialysis initiation for maintenance hemodialysis".

Yuzo Watanabe, Kunihiro Yamagata, Shinichi Nishi, Hideki Hirakata, Norio Hanafusa, Chie Saito, Motoshi Hattori, Noritomo Itami, Yasuhiro Komatsu, Yoshindo Kawaguchi, Kazuhiko Tsuruya, Yoshiharu Tsubakihara, Kazuyuki Suzuki, Ken Sakai, Hideki Kawanishi, Daijo Inaguma, Hiroyasu Yamamoto, Yoshiaki Takemoto, Noriko Mori, Kazuyoshi Okada, Hiroshi Hataya, Takashi Akiba, Kunitoshi Iseki, Tadashi Tomo, Ikuto Masakane, Tadao Akizawa, and Jun Minakuchi, for “Hemodialysis Initiation for Maintenance Hemodialysis” Guideline Working Group, Japanese Society for Dialysis Therapy

Role of iNOS and eNOS expression in a group of Egyptian diabetic and nondiabetic nephropathy patients

Abstract Introduction and aim Changes in renal nitric oxide (NO) production have been associated with glomerular hyperfiltration, vascular permeability, albuminuria, glomerulosclerosis, and tubulointerstitial fibrosis. This study aimed at detection of the role of both inducible nitric oxide synthases (iNOS) and endothelial nitric oxide synthases (eNOS) expression in diabetic and nondiabetic nephropathy patients. Methodology Renal biopsies and clinical data of 30 diabetic patients, 10 nondiabetic patients with renal impairment, and 10 control individuals were assessed for eNOS and iNOS expression. Results Both glomerular eNOS and iNOS expression levels were increased in diabetic nephropathy patients and this was associated with peripheral arterial occlusive disease. In nondiabetic patients, increased serum creatinine was found to be associated with increased iNOS and eNOS expression, and, together with the control group, they showed increased iNOS expression in tubular and interstitial cells. An association between cigarette smoking and increased expression of both iNOS and eNOS was detected in diabetic patients. Conclusion The presence of iNOS is associated with tubular damage resulting in renal failure. The upregulation of NO in diabetes mellitus type 2 may explain the endothelial dysfunction that is associated with almost all diabetic complications.

Effect of Renin-Angiotensin-Aldosterone System Triple Blockade on Non-Diabetic Renal Disease: Addition of an Aldosterone Blocker, Spironolactone, to Combination Treatment with an Angiotensin-Converting Enzyme Inhibitor and Angiotensin II Receptor Blocker

Although dual blockade of the renin-angiotensin-aldosterone system (RAAS) with the combination of an angiotensin-converting enzyme inhibitor (ACE-I) and angiotensin II receptor blocker (ARB) is generally well-established as a treatment for nephropathy, this treatment is not fully effective in some patients. Based on the recent evidence implicating aldosterone in renal disease progression, this study was conducted to examine the efficacy of blockade with three different mechanisms by adding an aldosterone blocker in patients who do not respond adequately to the dual blockade. A 1-year randomized, open-label, multicenter, prospective controlled study was conducted, in which 32 non-diabetic nephropathy patients with proteinuria exceeding 0.5 g/day were enrolled after more than 12 weeks of ACE-I (5 mg enalapril) and ARB (50 mg losartan) combination treatment. These patients were allocated into two groups of 16 patients each: a triple blockade group in which 25 mg of spironolactone daily was added to the ACE-I and ARB combination treatment, and a control group in which 1 mg of trichlormethiazide or 20 mg of furosemide was added to the combination treatment instead of spironolactone depending upon the creatinine level. After 1 year of treatment, the urinary protein level decreased by 58% (p<0.05) with the triple blockade but was unchanged in the controls. Furthermore, urinary type IV collagen level decreased by 40% (p<0.05) with the triple blockade but was unchanged in the controls. The decreases in urinary protein and urinary type IV collagen were not accompanied by a decrease in blood pressure. Mean serum creatinine, potassium and blood pressure did not change significantly by either treatment. In conclusion, triple blockade of the RAAS was effective for the treatment of proteinuria in patients with non-diabetic nephropathy whose increased urinary protein had not responded sufficiently to a dual blockade.

Impact of polymorphisms in the genes encoding xylosyltransferase I and a homologue in type 1 diabetic patients with and without nephropathy

Xylosyltransferase I (XT-I) is the chain-initiating enzyme in the biosynthesis of heparan sulfate proteoglycans (HSPGs). It catalyses the transfer of xylose to specific serine residues in the core protein. The XYLT-II gene codes for a protein highly homologous to the XT-I but its biologic function is not yet known. HSPGs are thought to play an important role in the permeability properties of the glomerular basement membrane (GBM) and thus the xylotransferase genes might be potential candidate genes predisposing to diabetic nephropathy in type 1 diabetic patients. We screened all XYLT-I and XYLT-II exons and flanking intron regions in 96 Caucasians with type 1 diabetes (48 with and 48 without diabetic nephropathy) using denaturing high-performance liquid chromatography (DHPLC). We also studied a nondiabetic control group. Applying this technique we identified 13 variations in XYLT-I and 20 in XYLT-II. The variations IVS6-9T>C and IVS6-14_IVS6-13insG in XYLT-II were found with a frequency of 5.2% (5/96) in nondiabetic nephropathy patients, while all nephropathy patients were negative (P= 0.06). Nondiabetic controls also showed the single nucleotide polymorphisms (SNP) at a frequency of 1.1% (5/440). The investigation of the SNPs' influence on clinical characteristics revealed significant associations for c.1989T>C (XYLT-I) and c.2402C>G (XYLT-II) with patients' blood pressure. We detected in our cohort associations between DNA sequence variations of genes encoding xylosyltransferases and the occurrence of altered clinical characteristics.

Addition of an angiotensin receptor blocker to full-dose ACE-inhibition: controversial or common sense?The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

Both angiotensin-converting enzyme (ACE)-inhibitors and angiotensin receptor blockers (ARBs) interfere with the activity of the renin-angiotensin system (RAS) in a different way. Theoretically, one might expect beneficial effects when they are used in combination, as a more complete suppression of the RAS can be achieved. But can this additional effect still be seen in patients on full-dose ACE-inhibition? Several controlled trials demonstrated that combination therapy can have additional benefits in hypertensive patients, in chronic heart failure patients, and in both diabetic and non-diabetic nephropathy patients. However, the clinical benefit was not always as pronounced as expected and not every patient will benefit from dual blockade of the RAS. There is some evidence of a less pronounced effect of combination therapy when a full dose of the ACE-inhibitor is given. However, it is well known that ACE-inhibitors cannot completely suppress the formation of angiotensin II, in particular, when the RAS is activated. Indeed, clinical trials indicated that add-on therapy with an ARB was especially of use when the RAS remained activated despite full-dose ACE-inhibitor treatment. In summary, combination of a full-dose ACE-inhibitor and an ARB can be a rational choice in selected patients.

Coronary artery bypass grafting in patients on chronic hemodialysis: surgical outcome in diabetic nephropathy versus nondiabetic nephropathy patients

Background. The presence of diabetes mellitus adversely affects the late survival of patients undergoing coronary artery bypass grafting (CABG). The purpose of this study is to clarify the role of diabetic nephropathy on outcomes of a group of patients on chronic hemodialysis undergoing CABG. Methods. Between April 1984 and July 1999, 45 patients on chronic hemodialysis underwent CABG. Forty-three had conventional CABG and 2 had off-pump CABG. There were 37 males and 8 females, and the mean age was 57 years (43 to 76 years). Twenty-one patients had diabetic nephropathy (group D) and 24 had nondiabetic nephropathy (group ND). Early and late results were determined in both groups. Results. Early outcome was not significantly different between the groups. There was no hospital mortality, stroke, or requirement for prolonged mechanical ventilation (>24 hours) in either group. No patients in group D, and only 1 (4.2%) in group ND had low cardiac output syndrome. The difference in the incidence of arrhythmias (23.8% in group D and 25% in group ND), wound infections (9.5% in group D and 8.3% in group ND), and delayed tamponade (5% in group D and 12.5% in group ND) was not statistically significant. However, late results differed significantly between the two groups. Actuarial survival (Kaplan-Meier) at 5 and 9 years was 22.9% and 11.5% in group D and 89.1% and 45.7% in group ND ( p = 0.01), respectively. Similarly, the cardiac event-free rate at the same intervals was 50.4% and 0% for group D and 100% and 65.8% for group ND ( p = 0.001), respectively. Conclusions. Using present technology, CABG can be done in patients on chronic hemodialysis with acceptable early mortality and morbidity. Late results in patients with diabetic nephropathy on hemodialysis are not as favorable as their nondiabetic cohort.

Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients.

Sodium-lithium countertransport (SLC) activity at a standard physiological sodium concentration is raised in uncomplicated IDDM, for which the kinetic mechanism is a raised maximum velocity (Vmax). Diabetic patients with nephropathy do not have raised values for Vmax but a low Michaelis constant (km). Transporter activity could be influenced by its membrane lipid environment. This was assessed in 21 control subjects, 32 uncomplicated diabetic patients, 17 patients with diabetic nephropathy and 11 patients with non-diabetic nephropathy by measuring the fluorescence anisotropy of DPH and TMA-DPH to assess different membrane regions. Standard SLC was higher in all the patient groups compared to the control subjects: 0.307 +/- 0.020 mmol Li/h x 1 cells in uncomplicated IDDM; 0.300 +/- 0.032 in diabetic nephropathy patients and 0.276 +/- 0.019 in non-diabetic nephropathy patients vs 0.216 +/- 0.011 mmol Li/h x 1 cells in control subjects (p < 0.001, p < 0.05, p < 0.05, respectively). This was due to raised Vmax values in the uncomplicated group: 0.528 +/- 0.035 vs 0.385 +/- 0.022 mmol Li/h x 1 cells in control subjects (p = 0.001) and low values for km in the diabetic nephropathy group: 58 (27-170) vs 106 (81-161) mmol/l in control subjects (p < 0.001). Raised SLC in the non-diabetic nephropathy group was largely due to raised Vmax: 0.460 +/- 0.030 mmol Li/h x 1 cells; p = 0.053, with no difference in km: 99.5 (74-137).(ABSTRACT TRUNCATED AT 250 WORDS)

Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients

Sodium-lithium countertransport (SLC) activity at a standard physiological sodium concentration is raised in uncomplicated IDDM, for which the kinetic mechanism is a raised maximum velocity (Vmax). Diabetic patients with nephropathy do not have raised values for Vmax but a low Michaelis constant (km). Transporter activity could be influenced by its membrane lipid environment. This was assessed in 21 control subjects, 32 uncomplicated diabetic patients, 17 patients with diabetic nephropathy and 11 patients with nondiabetic nephropathy by measuring the fluorescence anisotropy of DPH and TMA-DPH to assess different membrane regions. Standard SLC was higher in all the patient groups compared to the control subjects: 0.307±0.020 mmol Li/h x 1 cells in uncomplicated IDDM; 0.300±0.032 in diabetic nephropathy patients and 0.276±0.019 in non-diabetic nephropathy patients vs 0.216±0.011 mmol Li/h x 1 cells in control subjects (p<0.001, p<0.05, p<0.05, respectively). This was due to raised Vmax values in the uncomplicated group: 0.528±0.035 vs 0.385±0.022 mmol Li/h x 1 cells in control subjects (p=0.001) and low values for km in the diabetic nephropathy group: 58 (27–170) vs 106 (81–161) mmol/l in control subjects (p<0.001). Raised SLC in the non-diabetic nephropathy group was largely due to raised Vmax: 0.460±0.030 mmol Li/h x 1 cells; p=0.053, with no difference in km: 99.5 (74–137). DPH anisotropy was lower in the uncomplicated diabetic patients (0.210±0.0009) compared to the control subjects (0.214±0.0007: p=0.006) and was related to both standard SLC (rs=-0.68, p<0.001) and Vmax (rs= −0.77, p<0.001). Though DPH anisotropy in the diabetic nephropathy group was not different from normal control subjects, it also correlated with SLC (rs=-0.72, p<0.001) due to the same relationship with Vmax (rs=-0.73, p<0.001) as in uncomplicated diabetes. TMA-DPH anisotropy showed no difference between the four groups and was not related to either standard SLC, Vmax or km. Therefore, changes in membrane fluidity in the hydrophobic regions of the erythrocyte membrane may be responsible for some of the differences in SLC in IDDM.