Therapeutic nutrition for diabetic nephropathy

The development of diabetic kidney disease or diabetic nephropathy is accompanied by inhibition of normal kidney function. The state of functioning of the kidneys is assessed by the glomerular filtration rate (GFR). Every patient with chronic kidney disease wants information from their doctor about how to stop the progression of the disease.

Inhibition of the progression of nephropathy and risk reduction is based on 2 provisions that have the greatest evidence base:

• Optimize control of blood pressure figures
• Optimizing glucose control
• They have level of evidence A.

But apart from that, both doctors and patients have a lot of questions about nutrition. What should it be? How to determine therapeutic nutrition for diabetic nephropathy? How much power can you pause the process?

Nutrition can correct the levels of homeostasis in the body

So, it is known that the consumption of protein foods, namely animal origin, causes hemodynamic changes in the kidneys: renal blood flow and filtration in the glomeruli increase, renal vascular resistance decreases. Also, with increased protein intake, the content of advanced glycation end products increases. This causes fibrosis of the interstitium and also leads to the development of tubular atrophy.

Proteins of plant origin have a less pronounced burden on the kidneys, thereby less negatively affecting the hemodynamics of the kidneys. Also, plant proteins have cardioprotective, nephroprotective and anti-sclerotic effects.

Effect of a protein-free diet on disease progression

Based on clinical practice, there are many dietary guidelines regarding protein intake and protein restriction in the management of pre-dialysis patients with chronic kidney disease (CKD). Low protein diet - 0.7-1.1 g protein / kg per day, low protein diets - 0.3 g protein / kg per day.

The results of such diets have been mixed. However, recent observations make it clear that reducing protein in the diet does indeed have a modest positive effect.

Accordingly, a Cochrane systematic review of 40 studies in 2000 patients with CKD without diabetes mellitus found that when protein intake was reduced, the mortality rate fell by 34% compared with those patients who consumed increased or normal amounts of protein.

Keto diet expediency

There is evidence that the inclusion of essential amino acids, as well as their keto analogs (ketosteril), in a low-protein diet (LMP) has a positive effect on slowing down the progression of CKD. The introduction of such diets into the diet in the period before dialysis will not adversely affect subsequent replacement therapy.

In addition to the studies that have determined the appropriate use of ketosteril in CKD stages IV-V, the Hungarian pharmacoeconomic study of 2012 deserves attention. It showed the feasibility of early introduction of the keto diet into the life of the patient (CKD stage III) in comparison with the late start.

The keto diet is a non-protein diet (NBD) with ketosteril. It is used in the following dose - 1 tablet for every 5 kg of the patient's body weight per day. It is recommended to use this nutrition from an earlier date, with a decrease in GFR to 60 ml / min.

At an international congress on metabolism and nutrition in kidney disease, evidence was presented that the introduction of NBD into the diet is accompanied by only a small increase in the amount of phosphorus and nitrogenous waste compared to MBD. This effect suggests that the initial stages of renal replacement therapy are about a year later for some patients compared with MBD.

The addition of ketoacids makes it possible to increase insulin sensitivity of tissues, reduce lipid profile disorders, improve blood pressure control, reduce proteinuria and improve the quality of life of patients.

Properties of ketoacids

Keto acids, in addition to replacing the corresponding amino acids, also maintain nitrogen balance. Keto acids also have the following properties:

• retain nitrogen when the amino group changes into a keto acid. This is accompanied by suppression of ureagenesis;
• inhibit protein degradation, stimulate its synthesis. Thus, the use of leucine promotes protein synthesis;
• partially corrects the amino acid profile in uremic patients. This favorably affects the regulation of metabolic acidosis. In addition, the excretion of protein in the urine decreases against the background of diets with its restriction, as well as the consumption of keto / amino acids;
• serum albumin concentration increases;
• ketoacids do not lead to hyperfiltration of the kidneys;
• Metabolic acidosis as a result of improper excretion of hydrogen ions from sulfur-containing amino acids has a negative effect on protein metabolism. Glucose sensitivity and bone metabolism also change. Only a serious restriction or reduction of protein products can affect the correction of metabolic processes and acidosis;
• diets with limited intake of animal proteins reduce the consumption of phosphorus, and the presence of calcium has a positive effect on the pathologically altered metabolism of phosphorus and calcium, as well as on secondary hyperparathyroidism;
• Keto/amino acid therapy may improve some of the carbohydrate metabolism disorders that are seen in uremia. As a result, tissue sensitivity to insulin improves, and the concentration of circulating insulin decreases. The reduction of hyperinsulinemia with keto/amino acid therapy has a positive effect on the management of patients with uremia, especially those with insulin-dependent diabetes, obesity and CKD;
• keto/amino acid therapy has a positive effect on the correction of lipid disorders, especially triglycerides. This is important, since atherosclerosis is often observed in uremia. However, initiation of statin therapy in dialysis patients is not recommended (LE: 1B).

In our country, acid solution for parenteral administration is successfully used to correct ketoacidosis. Sometimes patients use it themselves.

In addition to protein restriction, people with DN are advised to reduce salt intake to 5-6 g/day. It is important to control the level of sodium in order to avoid a critical level of sodium in the blood, especially in elderly patients.

Pathological changes in calcium and phosphorus homeostasis, as well as the clinical picture of secondary hyperparathyroidism, progress depending on the decrease in GFR. The critical value is 60 ml/min. At this concentration, osteodystrophy, calcification of blood vessels and soft tissues develop, and the level of cardiovascular morbidity increases.

Therefore, it is worth introducing phosphate binders into the diet of patients with nephropathy. They bind phosphorus in the intestine, preventing it from being absorbed. The same fate awaits the active metabolites of vitamin D. This is due to the reduced ability of the kidneys in CKD to convert vitamin D to its active form.

Important things to remember about correcting hyperuricemia in patients with DN

Thus, restriction and reduction of protein intake in the diet of patients with DN is recommended. It is clinically and economically feasible to supplement nutrient deficiencies with ketoacids when GFR falls below 60 ml/min. It is necessary to correct sodium by medication and dietary, as well as vitamin D, phosphates, low-density lipids, calcium, control of body weight in order not to miss the lack of body weight.

It is possible to delay hemodialysis and progression of CKD in most patients. You just need to help them with this by talking about proper nutrition and lifestyle. After all, the main thing is the patient's confidence that he is acting correctly and is under the supervision of a competent specialist.

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