وصف
Chronic kidney disease involves a gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then removed in your urine. Advanced chronic kidney disease can cause dangerous levels of fluid, electrolytes and wastes to build up in your body. In the early stages of chronic kidney disease, you might have few signs or symptoms. You might not realize that you have kidney disease until the condition is advanced.Treatment for chronic kidney disease focuses on slowing the progression of kidney damage, usually by controlling the cause. But, even controlling the cause might not keep kidney damage from progressing. Chronic kidney disease can progress to end-stage kidney failure, which is fatal without artificial filtering (dialysis) or a kidney transplant
ملخص
- Chronic Kidney Disease (CKD) is defined by a glomerular filtration rate (GFR) less than 60 mL/min/1.73 m² persisting for over 3 months, with or without kidney damage signs. Kidney damage evidence includes proteinuria (albumin creatinine ratio > 30 mg/g) and pathological or structural abnormalities. Kidney failure, End-Stage Renal Disease (ESRD), and uremia, while often used interchangeably, are distinct. Kidney failure is a severe form of CKD where the kidney cannot maintain homeostasis of fluids, electrolytes, hormones, and metabolism. ESRD is CKD stage 5, requiring dialysis or kidney transplant. Uremia refers to the symptoms resulting from urea and creatinine buildup due to kidney failure.
- Diabetes and hypertension are the most common causes of CKD and ESRD. CKD ranks high among the top causes of death, but this is underestimated and increasing. Healthcare expenditure in India is low, with high private spending and low average spending per person compared to developed countries. Risk factors for CKD include diabetes, hypertension, family history of kidney disease, cardiovascular disease, HIV infections, autoimmune diseases, and recurrent infections.
- The kidney's primary functions include filtering blood, creating ultrafiltrate, selectively reabsorbing substances, and secreting substances into urine to maintain blood volume, electrolyte balance, and acid-base balance. It also produces hormones like erythropoietin and renin and activates vitamin D. Metabolic functions include gluconeogenesis and metabolizing drugs like insulin. CKD progression involves nephron loss, increasing stress on remaining nephrons and leading to endobi-metabolism, acidosis, and reactive oxygen species generation.
- Clinical manifestations include urine volume changes, elevated urea and creatinine (late stages), anemia and bone parameter changes (later stages), and impaired hormone catabolism. Common symptoms are nausea, vomiting, dyspnea, edema, restless legs, twitching, skin changes, and joint pain. Common signs include uremic fetor, pericardial rub, neuropathic changes, and hyperkalemia. Emergency indications for dialysis include breathlessness, severe acidosis, and fluid overload.
- CKD increases cardiovascular mortality due to mineral bone disorders, vascular calcifications, and elevated inflammatory cytokines. Non-traditional risk factors for cardiovascular disease in CKD include elevated cytokine markers, increased oxidation, advanced glycation end products, carbonyl stress, low futine levels, and abnormal mineral metabolism.
- Monitoring kidney function involves screening for albuminuria and calculating eGFR. GFR estimates nephron function, decreasing with nephron loss. Formulas for calculating GFR include MDRD and CKD-EPI, using readily available apps for computation. Creatinine measurements vary depending on the method used (JFS, ModFedJFS, IDMS). Albuminuria screening is recommended annually for all diabetic patients, using spot tests or 24-hour urine collection.
- Primary care physicians should advise weight reduction, high-fiber diets, regular exercise, limited alcohol, and sodium restriction for CKD patients. Blood pressure targets depend on albuminuria levels. ACE inhibitors and ARBs are first-line anti-hypertensives, but require monitoring for creatinine increases. Guidelines for diabetic control include HbA1c less than 7%.
- Medications commonly prescribed in primary care should be used cautiously or avoided in CKD patients due to risks of hyperkalemia and nephrotoxicity. These include ACE inhibitors, ARBs, potassium-sparing diuretics, and NSAIDs. Drug dosing often needs adjustment based on GFR. Referral to a nephrologist is warranted for rapid GFR decline, GFR below 45, atypical CKD progression, active urine sediment, uncontrolled hypertension, and significant proteinuria. Early nephrology referral decreases mortality. Patient education on CKD and its outcomes is crucial.
نموذج شهادة
حول المتحدثين
الدكتور ساتيانارايانا غاري
بكالوريوس الطب والجراحة، دكتوراه في الطب، دبلوم في طب الكلى، مستشفيات أبولو حيدر أباد
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