Compiled and authored by Pei Zhengxue

Research Progress on Renal Failure 2001.4.3

Chapter 1005

Some consider a serum creatinine concentration of 177 µmol/L as the irreversible threshold. When part of the nephrons are destroyed and the remaining nephrons compensate by enlarging and proliferating, they eventually re

From Compiled and authored by Pei Zhengxue · Read time 1 min · Updated March 22, 2026

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Section Index

  1. Research Progress on Renal Failure 2001.4.3

Research Progress on Renal Failure 2001.4.3

Some consider a serum creatinine concentration of 177 µmol/L as the irreversible threshold. When part of the nephrons are destroyed and the remaining nephrons compensate by enlarging and proliferating, they eventually reach a point where compensation is no longer possible—this is the theory of “correcting the imbalance.” This theory is currently supported by most scholars. In essence, it describes a state of high perfusion, high pressure, and high filtration in the surviving nephrons, which leads to the following pathological changes: ① Glomerular hypertrophy, with proliferation of endothelial and basement cells; ② Platelet aggregation within glomeruli and microthrombus formation, causing hypertrophied glomeruli to harden; ③ Increased glomerular permeability, with excessive increases potentially leading to protein loss in urine. These three changes further damage glomerular function. This vicious cycle is the common pathway for all cases of renal failure progressing to uremia. Recent studies have found that angiotensin II (Ang II) plays an important role in the progression of renal failure. Ang II is a potent vasoconstrictor with strong effects on renal blood vessels.

In recent years, in addition to increasing glomerular blood pressure, Ang II has also been found to promote vascular sclerosis in the glomerular matrix.

Risk factors for renal failure include hypertension, infection, nephrotoxic drugs, diabetes, high-protein diet, hormone use, hyperlipidemia, and elevated urinary protein.

Treatment strategies: ① Low-protein diet. Research shows that 0.6 g/(kg·d) of protein can meet the body’s basic protein needs; for an adult weighing 50 kg, 30 g of protein per day is sufficient (one egg contains about 60 g of protein). Note that starch and vegetables also contain some protein, and starch can even be converted into protein when necessary. Therefore, the body’s daily protein requirement is only about 20 g. The normal range for GFR (glomerular filtration rate) is 10–20 mL/min; those with higher GFR should increase protein intake, while those with lower GFR should reduce it. Insufficient protein intake will undoubtedly reduce essential amino acids (EAAs) in the blood. EAAs mixed with α-keto acids form an ideal formulation for long-term low-protein diets for patients with renal failure. α-keto acids combine with ammonia to produce EAAs, while also reducing urea formation. However, α-keto acids are expensive, and the usual dosage is 0.1–0.2/(kg·d).

In addition, ACEI use is also important. Captopril, Enalapril, and Bellapril are commonly used at a dose of 25 mg, taken 1–3 times daily.

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