Approach to a patient with raised creatinine - Copy.pptx

How to evaluate raised creatinine

1. Approach to a patient with raised creatinine Dr. emranul haque ( nahid ) Mbbs (mmc)

2. What is creatinine Creatinine is a waste product that is made by our muscles.Our kidneys work to filter creatinine as well as other waste products out of the blood.After being filtered ,these waste products are then expelled from our body in urine. Measuring creatinine levels can provide important insights about how our kidneys are functioning. Normal serum creatinine level 0.6-1.2 mg/dL

3. Conditions with raised creatinine 1.Renal failure(acute and chronic) 2.High Blood Pressure 3.Kidney infection 4.Glomerulonephritis 5.Heart Disease such as atherosclerosis or congestive heart failure 6.Blockage of the urinary tract 7.Drug toxicity 8.DM 9.Rhabdomyolysis

4. DRUGS THAT CAN CAUSE RAISED CREATININE 1.Anti-hypertensives mainly ACEIs And ARBs 2.NSAIDs 3.Antibiotics such as Aminoglycosides,Rifampicin,Vancomycin 4.Statins 5.Diuretics 6.Chemotherapy drugs

5. ACUTE KIDNEY INJURY Acute kidney injury(AKI), previously referred to as acute renel failure is the situation where there is a sudden and often reversible loss of renal function which develops over days or weeks and is often accompanied by a reduction in urine volume . Approximately 7% of all hospitalized patients and 20% of acutely ill patient develop AKI.In AKI associated with sepsis and multiple organ failure,mortality is 50%-70% .The outcome is usually determined by the severity of underlying disorder rather than kidney injury itself.Elderly patients are at higher risk of developing AKI and have a worse outcome.

6. Criteria for AKI

7. Causes of AKI

8. Rhabdomyolysis can cause AKI

9. Rhabdomyolysis

10. Acute Tubular Necrosis due to √ prolonged pre-renal state √ Sepsis

11. How….

12. How NSAIDs and ARBs cause AKI

13. Immediate clinical assesment History: √ Volume depletion ( vomiting,diarrhoea,burn,haemorrhage ) √ Drugs( diuretics,ACEIs,ARBs,NSAIDs ) √ Liver disease √ cardiac failure √H/o any immunosuppressive condition like DM,Iatrogenic cushing √H/o concealed blood loss following trauma especially fracture of the pelvis or femur and into the pregnant uterus.

14. Clinical features: √oliguria √anuria √ haematuria √ uraemic features such as anorexia,nausea √ dowsiness,confusion √muscle twitching √Increased Respiratory Rate √ Rash,weight loss,arthralgia √ flank pain

15. On Examination : √ BP-hypotension √Pulse- Tachycardia (Tachycardia and postural hypotension are valuable signs of early hypovolaemia ) √ signs of dehydration: Dry mucous membrane and increased skin turgor √ decreased urine output √ murmur,bilateral basal crepitation to exclude cardiac failure √fever with hypotension,wide pulse pressure,warm periphery to exclude septic shock √ Hypertension,edema , purpuric rash,uveitis,arthritis in case of GN √ Rectal examination:(prostate and anal tone), distended bladder,pelvic mass to exclude post renal causes.

16. Most AKIs are caused by pre-renal etiology (80%)

17. Investigations Serum creatinine :Raised Urine Na : < 20 mmol /L in pre-renal causes ;>40 mmol /L in renal causes Fractional excretion Na < 1% in pre-renal causes and >1% in renal causes Blood Urea: Raised Urea- creatinine Ratio:High Urine R/E: √ moderate to massive proteinuria,RBC,RBC Cast,Leukocyte in case of GN √ mild to moderate proteinuria,eosinophiluria (Hansel stain), leukocyte,WBC cast in case of AIN √ mild to moderate proteinuria , RBC,granular and hyaline cast in case of ATN

18. Contd. S. Electrolyte-dilutional hyponatraemia –if patient drink freely despite oliguria CBC with ESR CRP 24 hr urinary protein USG –bilateral swollen kidney in GN , corticomedullary differentiation,size of the kidney and to exclude post-renal cause S. calcium- low ,S. phosphate-high CXR to exclude cardiomegaly Renal Biopsy ANA,ANCA,C3,C4

19. Management of AKI

20. Chronic Kidney Disease It refers to an irreversible deterioration in renal function that usually develops over a period of years.Initially , it manifests only as a biochemical abnormality but,eventually ,loss of excretory,metabolic and endocrine functions of the kidney leads to the clinical symptomps and signs of renal failure,collectively referred to as uraemia . When death is likely without RRT(CKD stage 5),it is called end stage renal disease (ESRD). The prevalence of CKD stages 3-5 (eGFR<60 ml/min/1.73 m*2) are around 5-7%,mostly affecting people aged 65 years and above.

21. Pathophysiology Conditions Proportion Diabetes Mellitus 20-40% Interstitial Disease 20-30% Glomerular Disease 10-20% Hypertension 5-20% Systemic Inflammatory Disease 5-10% Renovascular Disease 5% Congenital and inherited 5% Unknown 5-20%

22. Stages of CKD

23. How we measure GFR and Equations of eGFR

24. Clinical features The typical presentation is for a raised urea and creatinine to be found incidentally during routine tests during screening of high risk patients (diabetes or hypertension). Most patients with slowly progressive disease are asymptomatic until GFR falls below 30. Some can remain asymptomatic with much lower GFR values than this. Patient may present with nausea,vomiting,loss of appetite , fatigue,weakness , sleep problems .

25. Contd. Nocturia √ an early symptom √ due to loss of concentrating ability ■ symptomps and signs are common -when GFR falls below 15-20 mL/min/1.73 m*2 and can affect almost all body systems. ■Tiredness or breathlessness due to renal anaemia or fluid overload. ●Elderly hypertensiv e patient if present with anaemia , it could be CKD ,so in this case CKD screening must be done.

26. Investigations..

27. Why anaemia in CKD ♂ Deficiency of erythropoietin ♂ Toxic effects of uraemia on marrow precursor cells ♂ Reduced red cell survival ♂ Blood loss due to capillary fragility and poor platelet function ♂ Reduced intake,absorption and utilization of dietary iron

28. Renal Osteodystrophy

29. Management of CKD The aims of management in CKD are to : -monitor renal function -prevent or slow further renal damage -limit complications of renal failure -treat risk factors for cardiovascular disease -prepare for RRT ,if appropriate

30. How.. By ABCDEF A- Correction of anaemia and albuminuria ( proteinuria ) B- Correction of BP and bacteria (infection –UTI) C-Correction of CHD & cigarette D- Correction of DM and drugs E- Correction of electrolyte imbalance and edema F-Correction of food and fluid.

31. Antihypertensive therapy and reduction of proteinuria ACEIs and ARBs- •All patients with diabetic nephropathy •CKD and proteinuria Irrespective of whether or not hypertension • Renal function checked within 7-10 days of initiating or increasing the dose of an ACEIs or ARBs. Adverse reactions of ACEIs and ARBs: it can increase serum potassium . √ Reminder: should not be commenced in patients with baseline potassium > 5.5 mmol /L ; should be discontinued if k+ > 6 mmol /L. And better to avoid potassium containing food like fruit juice,coconut water.

32. Target BP of a CKD patient Blood pressure 140/90 mmhg -CKD and no albuminuria . Blood pressure 130/80 mmhg -moderately elevated albuminuria . Blood pressure 125/75 mmhg,CKD and heavy proteinuria .

33. MaIntenance of fluid,electrolyte Acid-base balance Dietary advice Preventing excessive consumption of protein for all patients with stages 4 and 5 CKD. Hyperkalaemia ; - Avoid foods high in potassium - Potassium binding compounds ( Calcium resonium is not recommended, it can be associated with bowel necrosis) Diuretics- Frusemide , . Control of acidosis with sodium carbonate, √stopping or reducing drugs that elevate k+,such as potassium-sparing diuretics and ACEIs and ARBs;

34. Contd. If evidence of edema - Low sodium diet (< 100 mmol /24 hrs) -fluid intake should also be restricted. Diuretics, - increasing doses of potent loop diuretics or Synergistic combinations of loop , thiazide and potassium –sparing diuretics may be necessary.

35. Renal bone disease Management of renal bone disease should be two main driving factors, ► Hyperphosphatemia and inadequate activation of vitamin D ● Hyperphosphatemia prevention: - Dietary restriction of foods with high phosphate content ( milk,cheese,eggs and protein-rich foods) ♂ Phosphate-binding drugs. -Calcium Carbonate, - Aluminium hydroxide, - Lethanum carbonate and Sevelamer .(estimated serum phosphate level at or below 1.5 mmol /L)

36. Contd. Patients who are hypocalcaemic or have serum PTH more than twice the uper limit of normal: Active vitamin D metaboites , 1,25 – dihydroxyvitamin D In case of persistent hypercalcaemia parathyroidectomy may be needed. CKD with Anaemia – Recombinant human erythropoietin is very effective but risk of HTN and thrombosis Target Hb is usually between 100 and 120 g/L

37. When to refer to a nephrologist

38. “Don’t forget that as you age ,your kidneys also age and they demand more attention and care”