Nephropathy as a whole can be divided into five stages, in which the stage of renal insufficiency is in the middle stage, that is, the third stage of development, which is the key turning point of the whole disease development. In the first two periods, the basic problem of renal function damage is not big, and timely correction can completely recover. Patients who progress to the latter two stages not only have gradually serious renal function damage, but also have an accelerated pace and a significantly higher risk of renal failure.
Chronic renal insufficiency is caused by many reasons, with chronic renal parenchymal damage leading to azotemia, electrolyte disorder and acid-base imbalance as the main manifestations of clinical syndrome. The main causes are congenital diseases such as chronic pyelonephritis, chronic glomerulonephritis, hereditary nephritis and polycystic kidney disease.
Under the influence of renal insufficiency, the patient's glomerulus is seriously damaged, and there are problems in excreting metabolic waste, regulating acid-base balance and water-electrolyte balance, which will lead to this clinical syndrome. It can be divided into acute renal insufficiency and chronic renal insufficiency, which may threaten life and health if not adjusted in time.
Reducing urinary protein has always been a problem to be solved in the early stage of nephropathy. Most patients have active immune inflammatory reaction in the early stage, so urinary protein is the most important symptom affecting renal function. There is still a lot of proteinuria after some nephropathy develops to the stage of renal insufficiency, which has become an important factor to accelerate renal failure.
When renal function is incomplete, it often means that more than two-thirds of renal function is damaged, and the ability of kidney detoxification is obviously reduced. If you don't get timely and effective treatment at this time, the disease will continue to progress, and the late stage is called uremia.
Patients with renal insufficiency are prone to protein's failure. In order to make the intake of protein used by the human body to the maximum extent, it is metabolized to increase the burden on the kidneys. We should adopt a high-quality low-protein diet, consult a professional doctor, control the intake according to our own specific situation, and try to choose high-quality protein.
Pay attention to energy supplement in the process of high-quality low-protein diet, which requires 35 kilocalories per kilogram of body weight. The staple food is low-protein staple food, such as lotus root starch, crystal glutinous rice balls and silver needle powder. If you have diabetes at the same time, you need to control the amount of staple food.
After the kidney is damaged, some tissues and cells will die, which will lead to the blockage of some capillaries, which will lead to poor blood circulation in the kidney and reduce blood flow in the whole kidney. The kidney causes systemic blood flow to slow down, which in turn induces renal hypertension.
If it is not adjusted, the kidney will be in a high pressure state, which will undoubtedly accelerate renal failure. The increase of blood pressure in patients with renal insufficiency is irreversible, but it can be controlled. Therefore, antihypertensive drugs must be taken, and cannot be adjusted solely by diet and exercise.
Supplementing protein will inevitably lead to phosphorus intake, which is very unfavorable for patients with high creatinine. It has been reported that taking a very low phosphorus diet (65,438+0.4 of the normal phosphorus intake, equivalent to 300 ~ 350 mg/day) shows that the increase of serum creatinine in uremia patients has been controlled, and some of them have obviously decreased.
In order to reduce phosphorus intake, in addition to not eating phosphorus-rich foods (such as egg yolk, animal viscera, brain, bone marrow, etc.). Try to boil lean meat and fish in water before eating, or take calcium carbonate tablets to combine with phosphorus in the intestine and excrete it, thus reducing blood phosphorus.