Systemic manifestations in renal disease (95).pptx

Clinical features of Chronic kidney disease

1. SYSTEMIC MANIFESTAIONS in RENAL DISEASES Godwin D Fernandez 95

2. 1. Cardiovascular Abnormalities Cardiovascular disease is the leading cause of morbidity and mortality in patients at every stage of CKD. Between 30 and 45% of patients reaching stage 5 CKD already have advanced cardiovascular complications. Most patients with CKD succumb to cardiovascular disease before ever reaching stage 5 of CKD.

3. Ischemic Vascular Disease The increased prevalence of vascular disease in CKD patients derives from both traditional (classic) and non-traditional (CKD-related) risk factors Traditional risk factors Non-traditional risk factors Hypertension Hypervolemia Dyslipidemia Sympathetic overactivity Hyperhomocysteinemia Anemia Hyperphosphatemia Hyperparathyroidism Sleep apnea Generalized inflammation

4. The inflammatory state appears to accelerate the vascular occlusive disease and lower levels of Fetuin may permit more rapid vascular calcification, expectially in the face of hyperphosphatemia . Coronary reserve : Coronary reserve is also attenuated in CKD. Cardiac troponins levels are frequently elevated in CKD without evidence of acute ischemia. Increase in coronary blood flow in response to greater demand.

5. Heart faliure Heart faliure can be a consequence of diastolic or systolic dyfunction . A form of low pressure pulmonary edema can also occur in advanced CKD, manifesting a shortness of breath and a ‘bat wing’ distribution of alveolar fluid in the chest x –ray. Other CKD – related risk factors, including anemia , sleep apnea may contribute to the risk of heart failure.

6. Hypertension and Left ventricular hypertrophy Hypertension usually develops early during the course of CKD and is associated with adverse outcomes, includ ing the development of ventricular hypertrophy and a more rapid loss of renal function. Left ventricular hypertrophy and dilated cardiomyopathy are among the strongest risk factors for cardiovascular morbidity and mortal ity in patients with CKD . The use of exogenous erythropoiesis-stimulating agents can increase blood pressure and the requirement for antihypertensive drugs.

7. Pericardial disease Chest pain with respiratory accentuation, accompanied by a friction rub, is diagnostic of pericarditis. Classic electrocardiographic abnormalities include PR-interval depression and diffuse ST-segment elevation. Pericarditis can be accompanied by pericardial effusion that is seen on echocardiography and can rarely lead to tamponade . Pericarditis is observed in advanced uremia It is now more often observed in underdialyzed , nonadherent patients than in those starting dialysis.

8. 2. Disorders of calcium and phosphate metabolism The principal complications of abnormalities of calcium and phosphate metabolism in CKD occur in the skeleton and the vascular bed, with occasional severe involvement of extraosseous soft tissues. Bone manifestations in CKD - Classified into 2 ; High bone turnover disease with increased PTH levels (including osteitis fibrosa cystica , the classic lesion of secondary hyperparathyroidism) Low bone turnover disease with low or normal PTH levels ( adynamic bone disease and osteomalacia ).

9. P athophysiology of secondary hyperparathy - roidism and the consequent high-turnover bone disease declining GFR leads to reduced excretion of phosphate and, thus, phosphate retention the retained phosphate stimulates increased synthesis of PTH and growth of parathyroid gland mass . decreased levels of ionized calcium, resulting from diminished calcitriol production by the failing kidney as well as phosphate retention, also stimulate PTH produc tion .

10. Hyperparathyroidism stimulates bone turnover and leads to osteitis fibrosa cystica . Clinical manifestations of severe hyperparathyroidism include bone pain and fragility, brown tumors , compression syndromes, tumors , and erythropoietin resistance in part related to the bone marrow fibrosis. Low-turnover bone disease can be grouped into two categories ; Adynamic bone disease Osteomalacia Adynamic bone disease is characterized by reduced bone volume and mineralization and may result from excessive suppression of PTH production, chronic inflammation, or both.

11. In Osteomalacia there is accumulation of unmineral ized bone matrix that may be caused by a number of pro cesses , including vitamin D deficiency, metabolic acidosis, and in the past, aluminum deposition . Complications of adynamic bone disease include an increased incidence of fracture and bone pain and an association with increased vascular and cardiac calcification.

12. Calcium, phosphorus, and the CVS Hyperphosphatemia and hypercalcemia are associated wit h the increased vascular calcification . The magnitude of the calcification is proportional to age and hyperphosphatemia and is also associated with low PTH levels and low bone turnover. H yperphosphatemia can induce a change in gene expression in vascular cells to an osteoblast-like profile, leading to vascular calcification and even ossification.

13. Other complications of abnormal mineral metabolism Calciphylaxis (calcific uremic arteriolopathy ) is a devas tating condition seen almost exclusively in patients with advanced CKD. It is heralded by livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts . W arfarin treatment is considered a risk factor for calciphylaxis , and if a patient develops this syndrome, this medication should be discontinued and replaced with alternative forms of anticoagulation. Calciphylaxis

14. 3. Gastrointestinal and nutritional abnormalities Gastritis, peptic disease, and mucosal ulcerations at any level of the GI tract occur in uremic patients and can lead to abdominal pain, nausea, vomiting, and GI bleed ing . These patients are also prone to constipation, which can be worsened by the administration of calcium and iron supplements. The retention of uremic toxins also leads to anorexia, nausea, and vomiting. Protein-energy malnutrition , a consequence of low protein and caloric intake, is common in advanced CKD and is often an indication for initiation of renal replacement therapy. Assessment for protein-energy malnutri tion should begin at stage 3 CKD.

15. 4. Endocrine – Metabolic disturbances Glucose metabolism is impaired in CKD, as evidenced by a slowing of the rate at which blood glucose lev els decline after a glucose load. In women with CKD, estrogen levels are low, and menstrual abnormalities and inability to carry pregnan cies to term are common . Men with CKD have reduced plasma testosterone levels, and sexual dysfunction and oligospermia may supervene. Sexual maturation may be delayed or impaired in ado lescent children with CKD, even among those treated with dialysis.

16. Thank you