https://www.jrnjournal.org/article/S1051-2276(04)00135-9/pdf

Adequate protein dietary restriction in diabetic and nondiabetic patients with chronic renal failure.

The capacity to increase glomerular filtration rate in response to an acute oral protein load is known as the renal functional reserve; the loss of such capacity is used as a marker of hyperfiltration. This physiological response in obese hypertensives is not yet fully understood. We aimed to study the interdependent effects of obesity and hypertension on renal reserve, taking into account renal kallikrein and nitric oxide in the modulation of that parameter. Fourteen obese hypertensives (mean age, 50.5 +/- 0.9 years) and nine lean hypertensives (mean age, 50.6 +/- 2.7 years) were evaluated. Renal haemodynamics and the levels of serum nitric oxide and urinary kallikrein were assessed at baseline and after a protein load (1 g/kg of body weight). An increase in the following parameters was observed when comparing obese and lean hypertensives: basal glomerular filtration rate; renal plasma flow; and urinary kallikrein and nitric oxide levels (129.2 +/- 2.9 vs. 101.4 +/- 3.4 ml/min/1.73 m2; 587.5 +/- 18.2 vs. 502.8 +/- 16.7 ml/min/1.73 m2; 0.120 +/- 0.02 vs. 0.113 +/- 0.02 mU/ml; 23.2 +/- 0.8 vs. 19.5 +/- 1.2 mmol/ml, respectively). The renal reserve was lower in obese hypertensives when compared with that of lean hypertensives (4.1 +/- 0.5 vs. 11.8 +/- 0.8 ml/min, p < 0.005). After a protein load, contrasting with the lean group, inability to elevate the nitric oxide serum levels and a lower increase in urinary kallikrein were observed in the obese group. These data suggest that obese hypertensives lose renal reserve earlier in the evolution to renal dysfunction. This may be due to the defective modulation of renal vasodilatation mechanisms by renal kallikrein and nitric oxide production.

Renal functional reserve in obesity hypertension.

Oral administration of vanadate has a strong hypoglycemic effect but results in toxic side effects like life-threatening diarrhea. Tea is known to have potent antidiarrhea effects. We investigated the potential of suspending the vanadate in a tea decoction to reduce the diarrhetic action of vanadate. A concentrated extract of Lichee black tea was, therefore, added to sodium orthovanadate. Streptozotocin (STZ)-induced diabetic rats were orally gavaged with vanadate suspended in water or in the tea decoction, or with the tea extract alone. Blood glucose levels were assessed daily over 11 weeks with levels greater than 10 mmol/L warranting therapeutic intervention. Both the vanadate/water and vanadate/tea solutions acutely reduced blood glucose. The tea extract alone had no effect. The majority of vanadate/water-treated rats developed diarrhea and mortality rates approached 40%. Vanadate/tea-treated diabetic rats experienced no diarrhea or mortality and liver and kidney analyses (plasma ALT and creatinine, blood urea nitrogen [BUN], and urine-specific gravity) were normal. Animals treated with vanadate/tea retained blood glucose levels less than 10 mmol/L for an average of 24 consecutive days without subsequent treatments. Cataract formation was completely prevented. The mechanism of action of vanadate may have involved β-cell stimulation because vanadate/tea-treated diabetic rats exhibited normal plasma insulin levels. In summary, because of its long-lasting effects, oral administration, and lack of side effects, vanadate/tea represents a potentially important alternative therapy for an insuluin-defecient diabetic state.

Codelivery of a tea extract prevents morbidity and mortality associated with oral vanadate therapy in streptozotocin-induced diabetic rats

Long-Term Oral Intake of Low-Dose Cadmium Exacerbates Age-Related Impairment of Renal Functional Reserve in Rats

Protein wasting (PW) or protein-energy wasting (PEW) occurs commonly in patients with diabetes mellitus who have end-stage renal disease (ESRD) and are undergoing maintenance dialysis (MD) therapy. Some but not all studies indicate that PW or PEW is more prevalent in diabetic when compared with nondiabetic MD patients and that diabetic patients commencing maintenance hemodialysis (MHD) are more likely to lose fat-free, edema-free weight than are incident nondiabetic MHD patients. The causes of PW and PEW in diabetic MD patients are probably largely similar to those of nondiabetic MD patients. These causes include anorexia, reduced food intake, concurrent illnesses particularly when associated with inflammatory processes, physical or mental debility, removal of nutrients by dialysis procedure, acidemia, possibly physical deconditioning, and oxidant and carbonyl stress. However, diabetic MD patients are also at greater risk for PW or PEW from comorbidities related to diabetes per se. These disorders include ischemic vascular disease, hypertension, gastrointestinal dysfunction, and neuropathy. Metabolic disorders such as insulin deficiency or resistance to the actions of insulin, and elevated levels of counterregulatory hormones may also contribute to PW or PEW in diabetic MD patients. Mechanisms by which these metabolic disorders in diabetic ESRD patients may cause PW or PEW are discussed.

Effect of diabetes mellitus on protein-energy wasting and protein wasting in end-stage renal disease.

In poorly controlled diabetics, the whole-body protein flux is increased by 20-30% in comparison to well-controlled type I diabetes (IDDM) and normal subjects Intensive insulin administration completely reverses these abnormalities In poorly controlled IDDM, the primary effect of insulin administration is to reduce the increased protein catabolic rate by suppressing the accelerated rate of protein breakdown Studies in humans have demonstrated that the increased rate of protein synthesis observed in these patients is the consequence of elevated plasma amino acid levels When IDDM subjects develop renal complications, a protein-restricted diet may be recommended to preserve the remnant kidney function However, it has been demonstrated that in IDDM patients, metabolic adaptation to protein restriction is incomplete because suppression of endogenous proteolysis is impaired Since this component of protein metabolism is very sensitive to insulin action, maintaining strict metabolic control during the protein restriction regimen has been suggested The major studies on the effects of amino acid and insulin on protein metabolism in patients with diabetes mellitus are reviewed

Derangements in Protein Metabolism Induced by Type I Diabetes mellitus

Rationale. To establish relationship, if any, between renal morphology and renal haemodynamic response to amino acids. Design and methods. We investigated the correlation between renal haemodynamic regulation and morphology in a group of 15 patients with primary IgA nephropathy (IgAN) (age 26±2 years, BMI 24.4±1, GFR 64±5 ml/min, RPF 377±34 ml/min, FF 0.17±0.02). Twelve normal subjects (age 30±3 years, BMI 24±1, GFR 82±6 ml/min, RPF 421±42 ml/min, FF 0.19±0.02) were studied as controls. IgA patients were divided into two groups according to the histological staging of glomerular lesions : group I (n=7) stage II, and group II (n=8) stage III-IV. Results. In the basal state GFR was similar in the two groups and averaged 64 ± 9 and 64 ± 6 ml/min respectively. In contrast, FF was significantly lower in group II (0.14±0.01) (P<0.05) in comparison to group I (0.21±0.03) and controls (0.19±0.02). In order to evaluate the renal functional reserve, all study groups underwent to an intravenous amino-acid infusion designed to increase plasma amino acid levels twofold (total from 2096±145 to 4301±221 μmol/l in IgA nephropathy patients and from 2272±83 to 3844±238 μmol/l in controls). In response to amino-acid infusion, GFR rose significantly in group I (GFR 20±2% and RPF 37±4% versus basal) and controls (GFR 20±2% and RPF 20±3% versus basal) (both P<0.01 vs basal). In contrast, in patients with more severe glomerular lesions (group II) neither GFR nor RPF rose significantly (GFR -1±4% and RPF -8±6% versus basal) (P NS versus basal, P<0.01 versus group I and controls). Conclusions. The data show that in IgA nephropathy : severe forms of glomerular lesions are associated with a complex alteration of glomerular haemodynamic regulation, characterized by lower basal FF and loss of haemodynamic response to hyperaminoacidaemia.

Correlation between glomerular morphology and renal haemodynamic response to amino-acid administration in patients with IgA nephropathy

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Derangements in Protein Metabolism Induced by Type I Diabetes mellitus

Correlation between glomerular morphology and renal haemodynamic response to amino-acid administration in patients with IgA nephropathy