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CASE 1. Donald is a 68 year-old man who is admitted to hospital via the Emergency Department one day, following a myocardial infarction. Subsequent investigation.

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Presentation on theme: "CASE 1. Donald is a 68 year-old man who is admitted to hospital via the Emergency Department one day, following a myocardial infarction. Subsequent investigation."— Presentation transcript:

1 CASE 1

2 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 StageeGFR mL/min/1.73m 2 1>90 + persistent albuminuria 260 – 89+ persistent albuminuria 330-59 415-29 5<15 Hence this represents stage 3 CKD eGFR is estimated GFR and recommended to use MDRD (Modification of Diet in Renal Disease equation  more accurate than Cockcroft Gault among elderly and obese people and more accurate as kidney function declines) MDRD also contains factors to be applied to African American subjects

4 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)? Smoking Diabetes HTN Obesity Also review medications. Following drugs need to be reduced or ceased in people with CKD:  Colchicine (tubulin binding  for gout, as inhibits mitosis, neutrophil motility and activity)  Digoxin  Famciclovir  Gabapentin  Gibenclamide (sulfonylurea)  Glimepiride (sulfonylurea)  Lithium  Metformin  Sotalol  Valaciclovir  Triple whammy: NSAID/COX 2 inhibitor, ACE Inh, diuretic  Contrast  Aminoglycosides  Lithium

5 ACE Inh and ARB slows progression of CKD esp in pt with proteinuria (stop if creatinine rises 30% of baseline) MOA: Reduced glomerular capillary hydraulic pressure in combination with diminished size- and charge-selective properties of the glomerular capillary membrane are the most likely mechanisms involved in the antiproteinuric effect of ACE inhibitors.

6 Q.3. Briefly outline the key points in the relationship between kidney and cardiovascular disease Pt with CKD have substantial increase in cardiovascular risk that in part can be explained by increase in traditional risk factors such as HTN, diabetes, metabolic syndrome CKD alone is also independent risk factor for cardiovascular disease In CKD pt, risk of death is more due to cardiovascular disease (20 times greater) than requiring dialysis or transplantation

7 Q.4. Briefly outline the key points in your clinical action plan for this man. Goals: o Reduce progression of kidney disease o Reduce cardiovascular risk o Avoid & manage any complications o Any drugs that might damage kidney  avoid or adjust doses o Refer to Nephrologist when indicated Monitoring: 1 – 3 monthly clinical review, consisting: Clinical Ax: Blood pressure Weight Urine dipstick Laboratory Ax: Urea, creatinine, and electrolytes eGFR Fasting glucose Fasting lipids FBC Iron stores Ca and phosphate PTH (quarterly) Medications review

8 Q. 5. Why is it important to screen at-risk persons for CKD? 1.Because CKD is silent condition but can be readily detected with tests for proteinuria, hematuria, and eGFR 2.Symptoms of CKD may not appear until kidney function is severely impaired 3.CKD is potent independent risk factor for cardiovascular disease 4.Early intervention can reduce CKD progression and cardiovascular risk by 50% and improves quality of life

9 Q. 6 What symptoms of uremia may occur in ESRD? Malnutrition  due to anorexia, decreased intestinal absorption and digestion and metabolic acidosis Anorexia Nausea Vomitting Fatigue Sexual dysfunction Platelet dysfunction (uremic bleeding) due to uremic toxins. Increased uremia also increase NO synthesis  inhibitor of platelet aggregation Pericarditis Neuropathy (including encephalopathy, sensory dysfunctions)

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