Prevention and treatment of nonketotic hyperosmolar coma, lactic acidosis, and diabetic nephropathy

(1) Early detection and strict control of diabetes. The incidence of diabetes can gradually increase with age, especially in those over 50 years old, where it can reach more than 5%. Therefore, health care should be strengthened for the elderly or those in the pre-elderly stage, and blood glucose and urine glucose should be checked regularly during physical examinations to facilitate early detection and timely treatment.

(2) Prevention can avoid various inducing factors of this disease, such as infection, high fever, gastrointestinal diseases, etc. In particular, attention should be paid to those who are prone to severe dehydration in order to avoid hyperosmolar state.

(3) Use caution with any medications that may cause elevated blood sugar or dehydration.

Lactic acid is the final product of anaerobic glucose breakdown. Under normal circumstances, most lactic acid is converted into glycogen and stored in the liver, while a small portion is excreted through the kidneys to maintain metabolic balance. When lactic acid accumulates in the body and affects metabolism, serum lactic acid levels rise. When lactic acid exceeds 2 mg/L and the pH is less than 7.37, patients will experience discomfort, followed by nausea, vomiting, abdominal pain, shortness of breath, shock, and even coma. This condition is clinically known as lactic acidosis, and it often coexists with acute complications such as ketoacidosis. Lactic acidosis has a high mortality rate and is an acute complication of diabetes.

(1) Poor control of diabetes.

(2) Other acute complications of diabetes.

(3) Diseases of other vital organs.

(4) Taking large doses of biguanide. Patients may experience symptoms such as fatigue, nausea, vomiting, diarrhea, and upper abdominal pain. In severe cases, altered consciousness and coma may occur. Patients experiencing these symptoms should seek medical attention promptly. After diagnosis, alkali supplementation, oxygen therapy, and low-dose insulin supplementation should be administered. Dialysis may be necessary in some cases. It should be noted that patients with severe liver disease, kidney disease, or severe heart or lung dysfunction should avoid using biguanide hypoglycemic drugs.

(5) Others such as carbon monoxide poisoning, catecholamines, lactose overdose, etc.

Diabetic nephropathy is a general term for various types of kidney damage that occur as a complication of diabetes, and it is one of the leading causes of death in diabetic patients. In the early stages of diabetic nephropathy, there are few symptoms, and routine tests such as urinalysis will not detect protein, while serum creatinine and blood urea nitrogen levels are normal. Only with more sensitive methods can an increased rate of urinary microalbumin excretion be detected, often exceeding 20 micrograms per minute. As the disease progresses, it enters the clinical nephrotic stage, characterized by positive urine protein, gradually increasing serum creatinine and blood urea nitrogen levels, and a progressive decline in creatinine clearance, eventually leading to renal insufficiency. Patients present with significant proteinuria, hypertension, edema, anemia, and ultimately, even death.

The incidence of diabetic nephropathy is as follows: 33%–44% in type 1 diabetes and 15%–60% in type 2 diabetes. Microalbuminuria usually occurs 5 years after the diagnosis of diabetes, while massive proteinuria usually occurs 10 years after the diagnosis of diabetes. The average interval between the onset of proteinuria and death from uremia is 10 years, while those with more than 3.0 grams of protein in their urine per day generally die within 6 years.

(1) Strictly control blood sugar to keep it at a normal level.

(2) Strictly control blood pressure and use angiotensin-converting enzyme inhibitors. Options include captopril, enalapril, lisinopril, estazone, mononitrate, and estradiol. If blood pressure is still not well controlled, calcium channel blockers and other antihypertensive drugs can be added as appropriate. It is best to control blood pressure below 130/85 mmHg.

(3) A low-salt, high-quality protein diet is recommended because excessive salt intake can lead to high blood pressure and edema. Long-term high protein intake can increase the burden on the kidneys of diabetic patients and is detrimental to the kidneys.

(4) Regularly check the microurinary protein excretion rate in order to detect early diabetic nephropathy.

Stage I: This stage is characterized by glomerular hyperfiltration and hypertrophy at the time of diagnosis of diabetes.

Stage II: Kidney damage is present, but there are no clinical signs.

Stage III: This is the "high-risk stage" of diabetic nephropathy, typically occurring 10 to 15 years after the onset of diabetes.

Stage IV: The course of the disease is generally 15 to 25 years or more, with increased proteinuria, hypertension in most patients, and a decline in glomerular filtration rate.

Stage V: This is end-stage renal failure, commonly characterized by glomerular capillary occlusion, accompanied by glomerular hyalinization, very low glomerular filtration rate, nitrogen retention, and significant hypertension.

(1) Strictly control blood sugar. Intensive insulin therapy for type 1 diabetes can reduce the risk of diabetic nephropathy by 35% to 55%. Studies have shown that strict blood sugar control can also prevent and treat diabetic nephropathy in patients with type 2 diabetes.

(2) Control hypertension. Hypertension can accelerate the development of kidney failure. Effective antihypertensive treatment can slow the decline in glomerular filtration rate and reduce protein excretion in the urine. Blood pressure should be controlled below 130/80 mmHg.

(3) Limit protein intake. Appropriately reducing dietary protein (0.8 kg per day) can lower glomerular pressure, alleviate hyperfiltration, and reduce proteinuria. Conversely, a high-protein diet can worsen glomerular histological lesions. Those with existing renal insufficiency should further restrict protein intake and consume proteins containing essential amino acids.

(4) Dialysis and kidney transplantation. In the event of kidney failure, dialysis and kidney transplantation are the only effective treatments.

In the initial stages, glucosamine can be used. 5% of this drug is excreted through the kidneys, and 95% through bile. Other short- to medium-acting oral hypoglycemic agents, such as glibenclamide and omeprazole, can be chosen depending on the specific situation, but the dosage should be reduced. When using hypoglycemic tablets, the dosage should be small, and lactate should be monitored if possible. Hypoglycemic agents such as glibenclamide and glibenclamide are prone to hypoglycemia due to reduced excretion and accumulation in patients with renal insufficiency; therefore, they must be used with caution. Newly developed oral hypoglycemic agents such as acarbose, bismuth subcitrate, rosiglitazone, and pioglitazone can also be used in the early stages of diabetic nephropathy, but insulin therapy should be used in the later stages. Since the kidneys are also important organs for insulin metabolism and excretion, short-acting insulin therapy is best when renal function is severely impaired. The dosage should be small, and monitoring should be frequent to prevent hypoglycemia.