Chronic renal failure (CRF) is a syndrome caused by chronic progressive and irreversible damage to kidney function due to various reasons, characterized by the retention of uremic toxins, water-electrolyte imbalances, renal anemia, and disorders of calcium-phosphorus metabolism. Chronic renal failure represents the severe stage of renal insufficiency.

bubble_chart Diagnosis

1. Medical History and Symptoms

Patients often have a history of various glomerulonephritis, pyelonephritis, hypertension, diabetes, and pain wind disease. Early symptoms commonly include poor appetite, nausea vomiting, headache, lack of strength, and nocturia, gradually progressing to oliguria, edema, or high blood pressure. Many patients experience bad breath, oral membrane ulcers, nosebleeds, or gastrointestinal bleeding. Neurological and psychiatric symptoms such as difficulty concentrating, delayed reactions, limb numbness, drowsiness, or restlessness may occur. Severe cases may present with incontinence of urine or even unconsciousness. Chest tightness, shortness of breath, or discomfort in the precordial region suggests concurrent uremic cardiomyopathy. Cough, sputum production, or hemoptysis, along with inability to lie flat at night, indicates pulmonary edema or uremic pneumonia. A few patients may experience chest tightness, persistent precordial pain, or varying degrees of fever, possibly due to pericardial effusion. Symptoms like cutaneous pruritus, bone pain, or muscle spasms, even difficulty walking, suggest secondary hyperparathyroidism or renal osteodystrophy. Patients are prone to various infections, such as respiratory, urinary tract, or skin infections.

Most patients exhibit high blood pressure, anemia, or a dark complexion, with facial or lower limb edema. Abnormal mental status, systemic or localized bleeding, shallow or rapid breathing, orthopnea, jugular vein distension, dry or wet rales in the lungs, enlarged heart borders, pleural or pericardial friction rubs, changes in heart rate or rhythm, hepatomegaly, and ascites may be observed.

3. Laboratory Tests

(1) Urinalysis:

Decreased or fixed urine specific gravity, positive urine protein, and varying degrees of hematuria and casts.

(2) Blood tests:

Reduced hemoglobin and red blood cell count, decreased hematocrit and reticulocyte count, and in some cases, pancytopenia.

(3) Generation and transformation tests:

GFR 50–80 ml/min with normal blood urea nitrogen and creatinine indicates the compensatory stage of renal insufficiency; GFR 50–20 ml/min, serum creatinine 186–442 μmol/L, and urea nitrogen exceeding 7.1 mmol/L indicate the decompensated stage; GFR 20–10 ml/min, serum creatinine 451–707 μmol/L, and urea nitrogen 17.9–28.6 mmol/L indicate renal failure; GFR <10 ml/min, serum creatinine >707 μmol/L, and urea nitrogen >28.6 mmol/L indicate end-stage renal failure. Renal failure is often accompanied by hypocalcemia, hyperphosphatemia, and metabolic acidosis.

(4) Imaging studies:

Ultrasound shows reduced kidney size and enhanced cortical echogenicity. Radionuclide renal dynamic imaging reveals decreased glomerular filtration rate and impaired renal excretion. Bone scans may show renal osteodystrophy. Chest X-rays may reveal pulmonary congestion, pulmonary edema, increased cardiothoracic ratio, pericardial effusion, or pleural effusion.

4. Differential Diagnosis

For patients without a clear renal history and acute onset, differentiation from acute kidney failure is necessary. Severe anemia should be distinguished from gastrointestinal tumors or hematologic diseases. Additionally, identifying the primary disease and contributing factors is crucial to assess the extent of renal impairment.

bubble_chart Treatment Measures

The purpose of treatment is to alleviate symptoms and slow the progression of CRF. Specific measures are as follows:

1. Treatment of the primary disease:

Persist with long-term, rational treatment for primary or secondary glomerulonephritis, hypertension, diabetic nephropathy, etc.; avoid or eliminate factors that worsen CRF, such as hypovolemia, severe infections, urinary tract obstruction, and the use of nephrotoxic drugs.

2. Dietary therapy:

Caloric intake of 30–35 kcal/kg.d. During the compensatory phase of renal insufficiency, provide high-quality low-protein (0.6–0.8 g/kg.d), low-phosphorus (<750mg/d）飲食，必要時加用必需氨基酸或α-酮酸。晚期非透析的病人應予優質低蛋白飲食（<0.6g/kg.d）加用必需氨基酸或α-酮酸。

3. Control of hypertension:

ACE inhibitors and calcium channel blockers are the first choice, but care must be taken to prevent a functional decline in GFR. ACE inhibitors should be used cautiously or avoided in patients with serum creatinine levels above 350 μmol/L who are not undergoing dialysis. Diuretics, selective β-blockers, and angiotensin II receptor antagonists may be used as appropriate. For patients with early rapid deterioration of renal function, dopamine or prostaglandin E1 may be tried. For refractory hypertension, oral minoxidil, intravenous phentolamine, or nitroprusside may be used. For volume-dependent hypertension with heart failure, prompt dialysis is necessary. Avoid excessive or rapid blood pressure reduction; maintain blood pressure at around 16.0/11.3 kPa (120/85 mmHg).

Early dehydration should be treated with appropriate fluid replacement, but not excessively or too quickly. For oliguria, edema, and hypertension, restrict water and salt intake and intermittently administer intravenous furosemide. If the dose exceeds 400 mg/d without effect, discontinue use. Severe edema or heart failure should be treated with prompt dialysis for dehydration. For hyperkalemia, restrict potassium intake and manage according to "potassium metabolism disorders." If ineffective or in cases of anuria with myocardial damage, emergency hemodialysis is required. A few patients may have potassium deficiency and should be cautiously supplemented orally. For grade I metabolic acidosis, administer oral sodium bicarbonate. For severe acidosis, especially with deep breathing or unconsciousness, intravenous alkali therapy or emergency dialysis is needed to rapidly correct acidosis, along with intravenous calcium gluconate to prevent hand-foot spasm.

5. Toxin clearance therapy:

For mild cases, oral agents such as coated aldehyde starch, oral dialysis salts, uremic clearance, or renal failure-relieving medications may be used. Some patients may benefit from mannitol-salt water processing agents or Chinese herbal enemas. End-stage renal failure requires replacement therapy (dialysis or kidney transplantation); refer to relevant chapters.

6. Treatment of complications:

(1) For heart failure, actively address the underlying cause, restrict water and salt intake, administer intravenous furosemide, and use digitalis or vasodilators as appropriate. If ineffective, initiate dialysis as soon as possible.

(2) For cardiomyopathy, eliminate causative factors, correct anemia and electrolyte imbalances, control hypertension, and treat infections.

(3) Treatment for pericardial effusion depends on the cause. Effusions under 100 ml require no special treatment and can often be resolved with routine hemodialysis. For effusions caused by volume overload, strictly restrict water and salt and perform intensive dialysis with ultrafiltration for dehydration. For pericarditis due to inadequate dialysis and long-term metabolite retention, in addition to intensive dialysis, use high-efficiency dialyzers to remove middle-molecular-weight substances or parathyroid hormone, which is often effective. If cardiac tamponade occurs, perform emergency pericardiocentesis or pericardiotomy for drainage.

(4) Recombinant human erythropoietin (r-HuEPO) is a specific drug for treating renal anemia. The usual dosage is 50 U/kg, administered subcutaneously or intravenously three times per week. If the hematocrit increases by less than 0.03 or hemoglobin increases by less than 10 g/L after 4 weeks of treatment, the dosage should be increased to 5 U/kg to achieve a hemoglobin level of 100–120 g/L and a hematocrit of 33–38%. Subsequently, the maintenance dose should be adjusted to 50–100 U/kg, administered three times per week. Iron and folic acid supplementation should also be provided. For severe anemia (hemoglobin < 60 g/L) with significant symptoms, intermittent small-volume red blood cell transfusions may be considered. Kidney transplantation remains the most effective measure for treating renal anemia.

(5) For renal osteodystrophy, a low-phosphorus diet and oral phosphate binders should be prioritized, while hemodialysis can rapidly reduce blood phosphorus levels, which should be maintained between 1.4–2.4 mmol/L. Calcium supplements may be administered as needed to maintain normal blood calcium levels. Early intervention with 1,25(OH)₂D₃ at 0.25–1.0 μg/day or 1α(OH)D₃ at 0.5–2.0 μg/day is recommended.

(6) Symptomatic treatment: - For nausea and vomiting, oral medications such as Motilium, Prepulsid, or intramuscular injections of metoclopramide may be used. - For headache, insomnia, or dysphoria, sedatives like diazepam can be administered; calcium supplementation may be attempted for spasms. - For cutaneous pruritus, in addition to addressing calcium-phosphorus metabolic disorders, topical calamine lotion or oral chlorphenamine may be applied. - Patients with hyperuricemia should follow a low-purine diet and, if necessary, take allopurinol. Other measures include infection control and hemostasis.

(7) Traditional Chinese Medicine (TCM) and Chinese medicinals for pattern identification and treatment:

These can help alleviate symptoms and slow the progression of chronic renal failure (CRF). Some patients benefit from Chinese medicinals for purgation or lotion therapy, which may reduce the frequency of dialysis.