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HerbalAlchemist

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Lake Erie College of Osteopathic Medicine

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chronic kidney disease kidney disease medical study guide pathophysiology

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This document provides a study guide for nephrology exam 3 covering details of chronic kidney disease (CKD). It includes information on definitions, risk factors, pathophysiology, and complications of chronic kidney disease. This will be a useful resource for undergraduate medical students.

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Chronic Kidney Disease (CKD) Screening recommended for patients with DM, HTN, GU De nition: Progressive loss of renal function over months to abnormalities, autoimmune diseases, advanced age, or family...

Chronic Kidney Disease (CKD) Screening recommended for patients with DM, HTN, GU De nition: Progressive loss of renal function over months to abnormalities, autoimmune diseases, advanced age, or family years. history. ◦ Synonyms: progressive kidney disease; chronic renal Recommended Screening Tests: GFR estimation, urinary insuf ciency. albumin, urinalysis, and kidney imaging if necessary. Global impact: Estimated 850 million people affected. Signs: US Prevalence: Approximately 19 million people, about 11% of ◦ Cardiovascular: Edema, HTN, LVH, arrhythmia, dyslipidemia the population. ◦ Gastrointestinal: GERD, weight loss Categorization: Stages 1-5, based on kidney function level. ◦ Endocrine: Secondary hyperparathyroidism, gout, decreased ◦ Higher stage number indicates more advanced disease. vitamin D activation Risk Factors for CKD ◦ Hematologic: Anemia, iron de ciency, bleeding KI/DOQI (Kidney Disease Outcomes Quality Initiative) ◦ Fluid/Electrolytes: Hyper- or hyponatremia, hyperkalemia, categories: metabolic acidosis ◦ Susceptibility Factors: Correlated with, but not proven to Symptoms: directly cause, kidney damage. Useful for identifying high-risk ◦ Edema, cold intolerance, SOB, palpitations, cramping, muscle patients. pain, depression, anxiety, fatigue, sexual dysfunction. ▪ Examples: Advanced age, reduced kidney mass, low birth Complications of CKD weight, racial/ethnic minority, family history, low income, low Sodium and Water Homeostasis: Decreased ability to education, systemic in ammation, dyslipidemia. remove uid; ECF expansion may contribute to HTN. Sodium/ ◦ Initiation Factors: Directly cause kidney damage; modi able uid restriction may be needed in late stage IV and stage V. by pharmacologic therapy. Medications like corticosteroids, NSAIDs, androgens/ ▪ Examples: Diabetes mellitus, hypertension, glomerulonephritis estrogens, TZDs, and calcium channel blockers can contribute (autoimmune diseases), drug toxicity, urinary tract infections, to uid retention/edema. urinary stones. Potassium Homeostasis: Loss of ability to effectively remove ◦ Progression Factors: Associated with further kidney damage potassium; typically an issue in advanced CKD. Medications and decline in renal function. like ACE-I, aldosterone antagonists, potassium-sparing ▪ Examples: Hyperglycemia, uncontrolled hypertension, diuretics, ARBs, and potassium supplements can increase proteinuria, smoking, obesity. potassium. Pathophysiology of CKD Metabolic Acidosis: Common in advanced CKD; reduced Loss of nephrons. ammonia production impairs the ability to remove excess H+ Exposure to initiation factors. Anemia: Monitor hemoglobin levels; iron de ciency is a Hypertrophy of remaining nephrons leads to compensation and primary cause resistant to therapy. Evaluate for other causes of glomerular capillary hypertension. anemia. Iron de ciency manifests as microcytic anemia with Intraglomerular hypertension causes proteinuria. low MCV. Goals of therapy are to increase oxygen-carrying Angiotensin II mediates this process. capacity. Proteinuria and in ammatory cytokines promote progressive Secondary Hyperparathyroidism (sHPT) and Renal loss of nephrons and scarring of the interstitium. Osteodystrophy (ROD): Decreased renal function leads to Classi cation of CKD reduced phosphate excretion, resulting in increased PTH Based on Glomerular Filtration Rate (GFR) secretion and decreased levels of ionized calcium and ◦ Stage I: ≥ 90 mL/min decreased calcitriol. This leads to increased bone turnover and ◦ Stage II: 60-89 mL/min breakdown. ◦ Stage III: 30-59 mL/min Metabolic Acidosis: Goal is to normalize blood pH and ▪ IIIa: 45-59 mL/min maintain serum bicarbonate within normal limits; maintain pre- ▪ IIIb: 30-44 mL/min dialysis bicarbonate ≥22mEq/L in HD. ◦ Stage IV: 15-29 mL/min Pruritis: 60-90% of ESRD patients, multiple causes; treat with ◦ Stage V (ESRD): < 15 mL/min (including dialysis) antihistamines, 5-HT3 blockers, gabapentin. CKD-EPIcr is preferred for most patients. CKD-EPIcr-cys is Nutritional Status: Protein-energy malnutrition, vitamin and used if eGFR from CKD-EPIcr is suspected to be inaccurate. nutrition supplementation. Normal renal function may still have CKD if there is evidence of Uremic Bleeding: Usually mild but can be major; may attempt structural damage to the kidney. to treat with desmopressin, cryoprecipitate, estrogens. Quanti cation of Proteinuria Management of CKD Categories based on 24-hour collection or spot collection Goals: Delay progression of CKD, minimize complications. ◦ A1 (Normal): 150 minutes/week. Clinical Presentation of CKD ◦ Avoid sedentary behavior. Often asymptomatic until later stages, especially in stages I ◦ Maintain healthy BMI (18.5-24.9 kg/m2). and II. ◦ Limit dietary protein intake (0.8 g/kg/day in stages III-V). Minimal symptoms in stages III and IV. ◦ Limit sodium intake to

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