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UNUSUAL CASE OF ARF

UNUSUAL CASE OF ARF. Dr SAAD AL SHOHAIB KAUH. CASE PRESENTATION. 58 Y old Yemeni male Diabetic for 5 years with no obvious diabetic complications particularly no retinopathy Admitted with fever and pain in both legs for 4 days. CASE PRESENTATION.

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UNUSUAL CASE OF ARF

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  1. UNUSUAL CASE OF ARF Dr SAAD AL SHOHAIB KAUH

  2. CASE PRESENTATION 58 Y old Yemeni male Diabetic for 5 years with no obvious diabetic complications particularly no retinopathy Admitted with fever and pain in both legs for 4 days

  3. CASE PRESENTATION He had no other symptoms particularly no dyspnea cough or chest pain He had no GI symptoms and no urinary symptoms

  4. CASE PRESENTATION • P.M.H • Hypertension for 5 years on enalapril 5 mg once daily • No history of IHD

  5. Case presentation • Social history • Non smoker married 3 children

  6. Case presentation • On examination • He looked well B P 135/80 • Temp 38.5 pulse 90/min regular • JVP normal chest clear CVS normal • Abdomen normal

  7. Case presentation • Cellulitis both legs extending from ankles to both knees • No obvious collection • Good peripheral pulses • No evidence of peripheral nueropathy

  8. Case presentation • Lab work • WBC 17 Mainly nuetrophils Hb 13.1 • Na 138 K 4.1 urea 18 mmol/l • Cr 212 umol/l Ca 2.1 mmol/l P 1.6mmol/l • Urinalysis proteinuria no hemturia no casts • LFT normal

  9. Case presentation • Lab data • U/S normal size kidneys • C 3 and C4 normal • ANA negative • Hepatitis screen negative

  10. Course in hospital • Started on ceftrixone and clindamycin with his usual medications • His temprature subsided and cellulitis improved

  11. Course in hospital • His urine output had been maintained within normal range but his renal function got worse and finally his creatinine reached 1100 umol/l and urea 45 mmol/l • K 5.5 but no fluid over load • Dialysis was started

  12. Diff diagnosis • Post infectious GN • Drug induced • Pre existing diabetic nephropathy got worse with sepsis

  13. Kidney biopsy • Normal glomeruli • No interstilal infeltrate

  14. Course in hospital • He was dialysed for 10 days then his renal function stated to improve and creatinine decreased and reached normal value tow weeks after stopping dialysis • At that time he became polyuric for one week • He was sent home in good medical condition

  15. Post infectious G N • Immune complex nephritis can follow any bacterial viral fungal or parasitic infections • Can follow infected shunts and endocardits • May complicate deep abscesses • Usually present 3 weeks post infection

  16. Post infectious G N • Hematuria edema • Oliguria hypertension • Fever • Uncommonly ARF requiring dialysis

  17. NSAIDHEMODYNAMICALLY-MEDIATED ACUTE RENAL FAILURE • Although renal prostaglandins are primarily vasodilators, they do not play a major role in the regulation of renal hemodynamics in normal subjects • the release of these hormones (particularly prostacyclin and prostaglandin E2) is increased by underlying glomerular disease, renal insufficiency, hypercalcemia, and the vasoconstrictors angiotensin

  18. NSAIDHEMODYNAMICALLY-MEDIATED ACUTE RENAL FAILURE • Inhibition of prostaglandin synthesis with an NSAID in any of the above settings can lead to reversible renal ischemia, a decline in glomerular hydraulic pressure and ARF

  19. Any drug can induce AIN however it is seen more with antibiotics Affected patients typically present with hematuria, pyuria, white cell casts, proteinuria, and an acute rise in the plasma creatinine concentration. Fever, rash, eosinophilia, eosinophiluria – can be seen but not always present . Spontaneous recovery generally occurs within days weeks to a few months after therapy is discontinued ACUTE INTERSTITIAL NEPHRITIS

  20. Acute interstitial nephritis • The clinical picture is usually suggestive however the diagnosis is confirmed by renal biopsy • Gallium scan may be helpful • High dose steroid is useful to speed up recovery

  21. ATN • Any pre renal cause can lead to ATN if not corrected on time • The renal medulla is very sensitive to ischemia particularly in old dehydrated diabetic patients or those with CHF or liver cirrhosis • Nephrotoxic drugs would aggravate renal damage

  22. ATN • Mostly seen in the ICU setting • It is a clinical diagnosis • Biopsy is usually not indcated

  23. ATN • Fluid challenge is an important therapeutic and diagnostic approach • Examination of the urine Na and osmolarity are very important • The condition is potentially reversible but the mortality is still 50% since it happens in very sick patients

  24. Diabetic nephropathy • Diabetes is common in Saudi Arabia • This mainly related to genetic factors as well as the life style • 40% of patients with ERSD are diabetics

  25. Dialysis in Saudi Arabia • There are 6700 patients on dialysis in Saudi Arabia • There is 130 haemodialysis centres in Saudi Arabia • The incidence of hepatitis B is 6.7%and 50% for HCV SCOT data Saudi J kid 2001 12 (3)

  26. Diabetic nephropathy • Common problem 30 - 40% of dialysis patients are diabetics • Long standing diabetes • Genetic predisposition hypertension poor glycemic control are important risk factors • Strongly associated with retinopathy

  27. Diabetic nephropathy stages • Increased GFR and hyperfiltration • Normal GFR and mild mesangial expansion • Microalbumiuria • Overt proteinuria • CRF

  28. Diabetic nephropathy diagnosis • Clinical diagnosis • Long standing D M particularly in type 1 • Proteinuria or microalbumiuria • Retinopathy • Inactive urinary sediment • Normal sized kidneys

  29. Diabetic nephropathy • Microalbumiuria is a sign of cariovscular disease and is a very important finding since interference with strict glycemic control and ACE inhibitors is important • Strict glycemic control can reverse glomerular changes • Blood pressure control is vital and the ACE inhibitor dose should be titrated to the degree of proteinuria

  30. The Kidney’s

  31. Type 1 • Strict glycaemic control can decrease the nephropathy and progression of rena disese

  32. Type one DM It hasbeen suggested that 25 to 45 percent of these patients will, during their lifetime, develop clinically evident disease

  33. Strct blood pressure control is very imprtant • Genetic factors play major role in diabetic nephropathy • Most patients have retinopathy • Most are asymptomatic

  34. Urinary albumin excretion Normal excretion<30 mg/24 hrs (<20 µg/min) Microalbuminuria30–300 mg/24 hrs (20–200 µg/min) Clinical proteinuria>300 mg/24 hrs (>200 µg/min) Mogensen CE et al. Lancet 1995; 346: 1080–1084

  35. Microalbuminuria: Prevalence and predictive power in diabetics • Type 1 diabetes • Prevalence: 50% • Predictive value for the development of nephropathy: 75% • Type 2 diabetes • Prevalence: 25–60% (depending on ethnic origin) • Predictive value for the development of nephropathy: 25% Savage MW et al. Br J Hosp Med 1995; 54: 429–435 Viberti GC et al. In: International Textbook of Diabetic Medicine, 1992

  36. Serum creatinine level of 1.4 mg/dl:What is the renal function? 12 10 8 6 4 2 0 Large muscular male Normal male Small female Serum creatinine (mg/dl) 120 60 30 15 GFR (ml/min) 100 50 25 0 Fraction of normal renal function (%) Sica DA. Unpublished data

  37. ACE inhibitors in hypertension and heart failure In hypertension, ACE inhibitors • Lower blood pressure • Reduce the progression of end-organ damage In heart failure, ACE inhibitors • Improve cardiovascular hemodynamics • Improve symptomatolgy and exercise capacity • Decrease morbidity and mortality

  38. ACE inhibitors and renal impairment: Considerations ACE inhibitors ACE inhibitors show renoprotective effects over and above blood pressure control Dose modifications are a consideration in patients with renal impairment (except for fosinopril) Occasional cases of renal impairment and hyperkalemia have been reported with ACE inhibitors

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