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Week 26 Additional Renal Case 1 Shannon and Skye.

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Presentation on theme: "Week 26 Additional Renal Case 1 Shannon and Skye."— Presentation transcript:

1 Week 26 Additional Renal Case 1 Shannon and Skye

2 Trigger Donald is a 68 year-old man who is admitted to hospital via the Emergency Department one day, following a myocardial infarction. Subsequent investigation reveals that his eGFR is 42 mL/min/1.73m2. He comes to see you after his discharge, to discuss his kidney problem. Q.1 What stage of Chronic Kidney Disease (CKD) does this represent?

3 Stage 3 CKD – moderate decreased kidney function

4 No way to know this other than memorising /referring to this table…..

5 Q.2. What modifiable risk factors for CKD would you specifically seek in order to address them and slow progress to End Stage Renal Disease (ESRD)?

6 Modifiable risk factors for CKD Modifiable risk factors: the 4 biggies smoking Diabetes (blood glucose) high blood pressure Obesity Others (?) Cardiovascular risk reduction: –Lipids –Other lifestyle modification: physical activity, nutrition, alcohol Medication: nephrotoxic drugs, drug dosages appropriate for level of kidney function Non-modifiable risk factors: –age over 50 years –family history of kidney disease –Aboriginal or Torres Strait Islander heritage Q.3. Briefly outline the key points in the relationship between kidney and cardiovascular disease.

7 The presence of CKD is one of the most potent known risk factors for cardiovascular disease Individuals with CKD have a 10–20 fold greater risk of cardiac death than age and sex matched controls without CKD People with CKD are at least 20 times more likely to die from cardiovascular disease than survive to need dialysis or a transplant

8 Up-to-date Chronic kidney disease (CKD) alone is an independent risk factor for the development of coronary artery disease, and for more severe coronary heart disease (CHD) CKD is also associated with an adverse effect on prognosis from cardiovascular disease. This includes increased mortality after an acute coronary syndrome and after percutaneous coronary intervention (PCI) with or without stenting In addition, patients with CKD are more likely to present with atypical symptoms, which may delay diagnosis and adversely affect outcomes MECHANISM BEHIND RELATIONSHIP ? UNCLEAR Q.4. Briefly outline the key points in your clinical action plan for this man.

9 Based on modification of future cardiovascular risk. Recommended modalities include: Statin therapy Control of hypertension to below target of 140/90 mmHg (use ACEI/ ARB if proteinuric to below target of 130/80 mmHg). Low-dose Aspirin therapy Smoking cessation, maintenance of ideal body weight, tight glycaemic control etc Moniter eGFR three monthly Avoid nephrotoxic drugs, ensure drug doses appropriate Monitor/address common complications

10 Address the causes of CKD Treatment of reversible causes of renal dysfunction Decreased renal perfusion: Hypovolemia (V&D, diuretic use, bleeding), hypotension (MI or pericardial disease), sepsis, and NSAIDS, ACEI and diuretics etc that lower GFR. Ie. Hypovolemia may actually be present in CKD because diseased kidneys can’t resorb Na as well as they should – fluid replacement should be trialed if clinically dehydrated. Administration of nephrotoxic drugs: eg. Aminoglycosides, NSAIDS, vancomycin Urinary tract obstruction: Renal ultrasonography is often performed to exclude urinary tract obstruction in patients with an unexplained elevation in the serum creatinine. Preventing or slowing the progression of renal disease Glomerulosclerosis: Due to HTN in glomerulus, as well as metabolic acidosis and hyperlipidemia – ACEI/ ARB will slow/ prevent progression of CKD. (Statin therapy and smoking cessation helps too)

11 Treatment of the complications of renal dysfunction Volume overload: Tx with sodium restriction and diuretic therapy Hyperkalemia: Tx with Calcium chloride/ gluconate to protect heart, then lower serum K+ with glucose/ insulin, also use salbutamol and sodium bicarbonate acutely then institute potassium binding resins. Metabolic acidosis: Bicarbonate supplementation may slow the progression of both chronic kidney disease and resultant bone disease. Hyperphosphatemia: Reduction in ability to filter phosphate begins early in renal disease, and it’s affect on serum calcium causes PTH to be secreted – resulting in renal osteodystrophy. –Tx with dietary phosphate restriction and oral phosphate binders (when GFR <30ml/min) eg. Calcum carbonate, Sevelamer, Lanthanum, Aluminium hydroxide (not good), Calcium citrate etc. taken with meals. Anaemia: Normocytic normochromic, due to reduced EPO production by the kidney Tx with recombinant erythropoietin or darbepoetin alfa Q. 5. Why is it important to screen at-risk persons for CKD?

12 Therapeutic interventions implemented early in the course of CKD are effective in slowing or preventing the progression toward ESRD and its associated complications Q. 6 What symptoms of uremia may occur in ESRD?

13 Malnutrition — due to anorexia, decreased intestinal absorption and digestion, A low plasma concentration of albumin and/or creatinine (which varies with muscle mass as well as GFR) may be indicative. Uremic bleeding — Due to prolongation of the bleeding time, due primarily to impaired platelet function. Not normally treated unless patient is actively bleeding or about to undergo surgery etc Pericarditis — Fever, pleuritic chest pain, and a pericardial friction rub are the major presentations of uremic pericarditis, although other causes should be ruled out. Uremic neuropathy — Dysfunction of the central and peripheral nervous system, including encephalopathy (impaired mental status progressing if untreated to seizures and coma), polyneuropathy, and mononeuropathy are important complications of end- stage renal disease. They have become much less common because of the current tendency to earlier initiation of dialysis. Thyroid dysfunction — the kidney normally plays an important role in the metabolism, degradation, and excretion of several thyroid hormones. It is not surprising therefore that impairment in kidney function leads to disturbed thyroid physiology.

14 Other signs and symptoms include: –Decreased sense of smell and taste –Cramps –Restless legs –Sleep disturbances –hyperreflexia and Babinski reflex present –uremic fetor –nausea/vomiting –Amenorrhea and sexual dysfunction –Reduced body temperature

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