47 Complications of CKD Habib Shafi.pptx

Complications of CKD

1. Complications of CKD Mawlana Habib Shafi Niazi

2. Complications Cardiac Bone AND Minerals Hematologic Hyperkalemia Acid-base disorders Neurologic endocrine

3. Cardiac Complications HTN CAD HF Afib Pericarditis

4. HTN in CKD most common complication of CKD; progressive and salt-sensitive control of hypertension should focus on both pharmacologic and nonpharmacologic therapy ( eg , diet, exercise, weight loss , treatment of obstructive sleep apnea ) low salt diet (2 g/day ) Diuretics needed to control HTN Initial drug therapy for proteinuric patients should include ACE inhibitors or ARBs

5. HTN in CKD ACEi and ARB patients must have serum creatinine and potassium checked within 7–14 days. A rise in serum creatinine greater than 30 % from baseline mandates reduction or cessation of the drug should not be used in combination BP Goal 130/80

6. CAD higher risk for death from CVD than the general population. Traditional modifiable risk factors for CVD , such as hypertension, tobacco use, and hyperlipidemia, should be aggressively treated in patients with CKD . Uremic vascular calcification involving disordered phosphorus homeostasis and other mediators may also be a cardiovascular risk factor in these patients

7. Atrial Fibrillation 20% prevalence in patients receiving dialysis. Rate and rhythm management should be addressed.

8. Heart Failure due to hypertension, volume overload, and anemia accelerated rates of atherosclerosis and vascular calcification resulting in vessel stiffness LVH and HFpEF Diuretics and Salt Restriction ACE inhibitors and ARBs can be used for patients with advanced CKD with close monitoring of blood pressure as well as for hyperkalemia and worsening kidney function

9. Pericarditis uremic patients; typical Findings :pleuritic chest pain and a friction rub. significant pericardial effusion may result in pulsus paradoxus , an enlarged cardiac silhouette on chest radiograph, and low QRS voltage and electrical alternans on ECG . The effusion is generally hemorrhagic, and anticoagulants should be avoided if this diagnosis is suspected. Cardiac tamponade can occur; therefore, uremic pericarditis is a mandatory indication for hospitalization and initiation of hemodialysis

10. Disorders of Mineral Metabolism metabolic bone disease of CKD refers to the complex disturbances of calcium and phosphorus metabolism, parathyroid hormone (PTH), active vitamin D, and fibroblast growth factor-23 (FGF-23) homeostasis

11. typical pattern seen as early as CKD stage 3 is hyperphosphatemia , hypocalcemia, and hypovitaminosis D, resulting in secondary hyperparathyroidism

12. Bone disease, or renal osteodystrophy , in advanced CKD is common and there are several types of lesions. Renal osteodystrophy can be diagnosed only by bone biopsy, which is rarely done. The most common bone disease, osteitis fibrosa cystica , is a result of secondary hyperparathyroidism and th osteoclast stimulating effects of PTH high-turnover disease with bone resorption and subperiosteal lesions; it can result in bone pain and proximal muscle weakness

13. Adynamic bone disease, or low-bone turnover, is becoming more common ; it may result iatrogenically from suppression of PTH or via spontaneously low PTH production Osteomalacia is characterized by lack of bone mineralization treatment may involve correction of calcium, phosphorus , and 25-OH vitamin D levels toward normal values, and mitigation of hyperparathyroidism

14. Declining GFR leads to phosphorus retention. This results in hypocalcemia as phosphorus complexes with calcium, deposits in soft tissues, and stimulates PTH. Loss of renal mass and low 25-OH vitamin D levels often seen in CKD patients result in low 1,25(OH ) vitamin D production by the kidney. Because 1,25(OH) vitamin D is a suppressor of PTH production, hypovitaminosis D also leads to secondary hyperparathyroidism

15. first step in treatment of metabolic bone disease is control of hyperphosphatemia dietary phosphorus restriction initially ( see section on dietary management oral phosphorus binders if targets are not achieved Oral phosphorus binders block absorption of dietary phosphorus in the gut and are given thrice daily with meals

16. Calcium containing binders (calcium carbonate, 650 mg/tablet, or calcium acetate, 667 mg/capsule , used at doses of one to three pills per meal) are relatively inexpensive but may contribute to positive calcium balance and vascular calcification ; overt hypercalcemia may also occur current guidelines suggest limiting their use in favor of the non-calcium–containing binders sevelamer carbonate (800–3200 mg/meal) and lanthanum carbonate ( 500–1000 mg/meal )

17. Phosphate Binders Once serum phosphorus levels are controlled, active vitamin D ( 1,25[OH] vitamin D, or calcitriol) or other vitamin D analogs are used by nephrologists to treat secondary hyperparathyroidism in advanced CKD and ESRD. Serum 25- OH vitamin D levels should be measured and brought to normal prior to considering administration of active vitamin D

18. Typical calcitriol dosing is 0.25 or 0.5 mcg orally daily or every other day. Cinacalcet targets the calcium-sensing receptors of the parathyroid gland and suppresses PTH production. Cinacalcet , 30–90 mg orally once a day, can be used if elevated serum phosphorus or calcium levels prohibit the use of vitamin D analogs; cinacalcet can cause serious hypocalcemia, and patients should be closely monitored for this complication

19. Hematologic Complications CKD Anemia Coagulopathy

20. Anemia in CKD due to decreased erythropoietin production Anemia Of Chronic Disease: high levels of hepcidin , which blocks GI iron absorption and mobilization of iron from body stores thyroid function tests, serum vitamin B 12 levels, and iron stores (ferritin and iron saturation) should be checked In CKD, a serum ferritin below 100–200 ng/mL or iron saturation less than 20% is suggestive of iron deficiency

21. Iron stores may be repleted with oral or parenteral iron; iron therapy should probably be withheld if the serum ferritin is greater than 500–800 ng/mL, even if the iron saturation is less than 20 %. Oral therapy with ferrous sulfate, gluconate, or fumarate, 325 mg once daily , is the initial therapy In pre-ESRD CKD those who do not respond due to poor GI absorption or lack of tolerance, intravenous iron ( eg , iron sucrose or iron gluconate ) may be necessary

22. Erythropoiesis-stimulating agents (ESAs, eg , recombinant erythropoietin [ epoetin alfa or beta] and darbepoetin ) are used to treat the anemia of CKD if other treatable causes are excluded starting dose of epoetin alfa is 50 units/kg (3000–4000 units/dose) once or twice a week, and darbepoetin is started at 0.45 mcg/kg and administered every 2–4 weeks; epoetin beta is given every 2–4 weeks

23. ESAs Intravenous Subcutaneous darbopoetin Hypertension is a common complication of treatment with ESAs

24. Coagulopathy bleeding diathesis that may occur in stage 4–5 CKD is mainly due to platelet dysfunction Treatment is required only in patients who are symptomatic Desmopressin (25 mcg intravenously every 8–12 hours for two doses ) is a short-lived but effective treatment for platelet dysfunction and it is often used in preparation for surgery or kidney biopsy Dialysis improves the bleeding time

25. Hyperkalemia stages 4–5 Cardiac monitoring is indicated for any ECG changes seen with hyperkalemia or a serum potassium level greater than 6.0–6.5 mEq /L or mmol /L Chronic hyperkalemia is best treated with dietary potassium restriction (2 g/day) and minimization or elimination of any medications that may impair renal potassium excretion Diuretics

26. Acid Base Disorders Damaged kidneys are unable to excrete the 1 mEq /kg/day of acid generated by metabolism of dietary animal proteins in the typical Western diet Metabolic Acidosis Decreased GFR proximal or distal tubular defects may contribute to or worsen the acidosis Excess hydrogen ions are buffered by bone; the consequent leaching of calcium and phosphorus from the bone contributes to the metabolic bone disease

27. Chronic acidosis can also result in muscle protein catabolism as well as growth retardation in children with CKD and may accelerate progression of CKD Reduction of dietary animal protein and increased fruit and vegetable intake, and the administration of oral sodium bicarbonate (in doses of 0.5–1.0 mEq /kg/day divided twice daily and titrated as needed) are strategies to bring serum bicarbonate levels toward normal

28. Neurologic Complications Uremic encephalopathy does not occur until GFR falls below 5–10 mL/min/1.73 m2 Symptoms begin with difficulty in concentrating and can progress to lethargy, confusion, seizure, and coma . Physical findings may include altered mental status, weakness, and asterixis . These findings improve with dialysis peripheral neuropathies (stocking-glove or isolated mononeuropathies ), erectile dysfunction, autonomic dysfunction, and restless leg syndrome These may not improve with dialysis therapy

29. Endocrine Complicaions Decreased renal elimination of insulin in advanced CKD confers risk for hypoglycemia in treated diabetic patients Doses of oral hypoglycemics and insulin may need reduction. The risk of lactic acidosis with metformin is due to both dose and eGFR ; it should be discontinued when eGFR is less than 30 mL/min/1.73 m2 Decreased libido and erectile dysfunction are common

30. Men have decreased testosterone levels; women are often anovulatory . Women with serum creatinine less than 1.4 mg/ dL are not at increased risk for poor outcomes in pregnancy; however, those with serum creatinine greater than 1.4 mg/ dL may experience faster progression of CKD with pregnancy pregnancy can occur in this setting; however, fetal mortality approaches 50%, and babies who survive are often premature

31. Treatment

32. Anemia Initiate iron therapy if TSAT ≤ 30% and ferritin ≤ 500 ng/mL (IV iron for dialysis, Oral for non-dialysis CKD) Individualize erythropoiesis stimulating agent (ESA) therapy: Start ESA if Hb <10 g/dl, and maintain Hb <11.5 g/dl. E nsure adequate Fe stores. Appropriate iron supplementation is needed for ESA to be effective

33. CKD-Mineral and Bone Disorder (CKD-MBD) Treat with D3 as indicated to achieve normal serum levels 2000 IU po qd is cheaper and better absorbed than 50,000 IU monthly dose. Limit phosphorus in diet (CKD stage 4/5), with emphasis on decreasing packaged products - Refer to renal RD May need phosphate binders

34. Detect and Manage CKD Complications Metabolic acidosis Usually occurs later in CKD Serum bicarb >22mEq/L Correction of metabolic acidosis may slow CKD progression and improve patients functional status 1,2 Hyperkalemia Reduce dietary potassium Stop NSAIDs, COX-2 inhibitors, potassium sparing diuretics ( aldactone ) Stop or reduce beta blockers, ACEi /ARBs Avoid salt substitutes that contain potassium

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