22 - Acute and chronic kidney failure.pptx

Most medical students graduate without knowing the diagnosis and management of acute and chronic kidney failure. Renal units requires you to have a thorough knowledge. So this presentation will assist you to have such knowledge

1. Acute and chronic kidney failure

2. 1. Acute kidney injury (AKI) 1.1 Definition: Acute onset, rapid deterioration of kidney function over hours/days Subsequently azotaemia (=retention of nitrogenous waste products) and disturbance of fluid, electrolyte, and acid-base balance Chief symptom: olig- / anuria and increase of serum creatinine >50% of initial value Oliguria: <500 ml/day; anuria : <100 ml/day But: up to 30% of AKI present with normal or even increased urine output (polyuria) 1.2 Epidemiology: no reliable data from SSA; globally 3-10% of hospitalised patients, with mortality of 20% (50% in ICU patients)

3. 1.3 Etiology

4. 1.3.1 Pre-renal AKI 60% of all cases Caused by reduced renal perfusion: Volume depletion (blood loss, dehydration, extensive burns, pancreatitis) Reduced cardiac output / circulatory failure (acute MI, pulmonary embolism, burns, major surgery) Systemic vasodilation (sepsis) Renal vasoconstriction (hepato-renal syndrome in liver cirrhosis In principle, pre-renal AKI is reversible if causing factors are removed / treated

5. 1.3.2 Post-renal AKI 5% of cases In principle reversible if cause is removed / treated Caused by obstruction of efferent urinary passage: (Congenital malformations) Tumours (benign/malign), stones BPH, gynaecologic diseases / postop complications Misplaced or obstructed urinary catheters Drugs (neuroleptics etc.)

6. 1.3.3 Renal AKI 35% of cases Prognosis depends on underlying condition Acute GN (5% of cases) Acute tubular necrosis (85% of cases) Ischaemic Toxic (drugs such as aminoglycosides, amphotericin B, contrast dye; haemolysis; tumor-lysis syndrome) Acute interstitial nephritis (10% of cases) Drugs (penicillines, NSAIDS, sulfonamides) Systemic diseases (SLE ) Infiltration (leukaemia, lymphoma)

7. 1.4 Signs and symptoms Clinical features may be very unspecific Main dangers are: Fluid overload (cardiac failure, brain oedema) Hyperkaliaemia, acidosis, uraemia Complications: RS: pulmonary oedema, pneumonia, ARDS CVS: pericarditis, arrhythmia, HTN CNS: convulsions, confusion, coma GI: haemorrhagic gastritis Haematologic: bleeding, anaemia Infections

8. 1.5 Diagnostic Laboratory: U&Es, FBC Urinalysis: Unremarkable in pre- and post-renal causes RBC casts in acute GN («Nephritic sediment») WBC casts in acute interstitial nephritis Muddy brown casts in acute tubular necrosis Additional tests, if available: ANA, ANCA, CK, etc. Imaging: USS: To rule out obstruction Kidneys usually large in AKI Doppler may show impaired perfusion

9. 1.5 Diagnostic ctd. Urinalysis – casts : WBC cast RBC cast Muddy brown casts

10. 1.6 Management Treatment of underlying cause! Avoidance of further injuries! Symptomatic treatment: Monitor fluid and electrolyte balance, restrict potassium Restrict fluid intake in anuria: extrarenal loss + 600 ml Adjust dosage of drugs Loop diuretics may be tried but have to be discontinued in case of anuria (adverse effects) No protein restriction (only in nephrotic syndrome!) Indications for dialysis: Fluid overload Refractory hyperkaliaemia Symptomatic uraemia

11. 2. Chronic kidney failure (disease, CKD) 2.1 Definition: reduction of GFR* <60 ml/min for > 3months Classified in stages 1-5, whereas 1 and 2 are >60 ml/min; Stage 3: 30-59 ml/min Stage 4: 15-29 ml/min Stage 5 = end stage (ESRD): <15 ml/min or dialysis 2.2 Epidemiology : prevalence in SSA is estimated at 13.9% (but lack of reliable data ) *Reminder: GFR is the total amount of blood filtrated by the kidney (expressed in ml/min) Cockcroft-Gault equation:  

12. 2.3 Etiology Commonest cause is diabetic nephropathy (35% in developed countries) Primary and secondary GN Vascular (hypertensive) nephropathy Polycystic kidney disease HIV nephropathy Toxic (e.g. analgesic nephropathy) Chronic tubulo-interstitial kidney disease

13. 2.4 Pathophysiology Consequences of CKD include: Failure of excretory function Initially osmotic diuresis with polyuria Disturbance of fluid, electrolyte, and acid-base balance Salt and water retention, hyperkaliaemia, acidosis Ca-release from bones, increased protein katabolism Impaired incretory function Renal anaemia (lack of EPO), renal osteopathy (vit D deficiency) Toxic organ damage Azotaemia results in end organ damage, especially on CVS Risk of cardiovascular events is markedly increased

14. 2.5 Signs and symptoms Early symptoms: polyuria, peripheral oedema, HTN Late symptoms: fatigue, pallor, headache, nausea, pruritus End-stage symptoms: vomiting, dyspnoea, olig-/anuria, encephalopathy (drowsiness, convulsions, coma), bleeding tendency (thrombocytopathy/-penia) Uraemic foetor Pulmonary congestion («fluid lung»), pericardial and/or pleural effusion Muscle fibrillations (myopathy) Paraesthesia (uraemic PNP) Infections (immunosuppression)

15. 2.6 Diagnostic Should aim to rule out reversible causes of CKD Laboratory: Urea, Creatinine, electrolytes (including calcium, phosphate) Urinalysis and sediment Ideally: collect urine over 24 hours for Creatinine-Clearance and total protein FBC Blood gas analysis Additional tests, if available: ANA, ANCA, CK, etc . Imaging: USS, angio MRI Other: Kidney biopsy

16. 2.7 Management Indicators for rapid progression are DM, HTN, hyperlipidaemia, hyperuricaemia, proteinuria, smoking, anaemia A: Conservative treatment: Avoid nephrotoxic drugs/substances Adjust dosage of medication Aim to keep BP in low-normal range (≤140/90 if no albuminuria, ≤130/80 if albuminuria present) Diet: protein restriction to 0.8g/kg; appropriate calories (>2000kcal/day); salt restriction only if oedema and/or HTN Initially increased fluid intake (2-2.5L/day) Monitoring of electrolytes and acid-base balance Treatment of renal anaemia, renal osteopathy Treatment of cardiovascular risk (statins)

17. 2.7 Management ctd. B: Dialysis: Is indicated in case of uraemic symptoms, fluid overload, hyperkaliaemia, refractory acidosis, refractory HTN In the absence of any of the above it is indicated in GFR <7mL/min Commonest method is intermittent haemodialysis (HD) (3x weekly for 4-8 hours) via AV-fistula Alternative is peritoneal dialysis (PD) over night C: Kidney transplantation Treatment of choice for ESRD, but obviously limited availability (of organs as well as experienced surgeons) Requires subsequent immunosuppression with associated problems

18. 2.7 Management ctd. Complications of HD and of CKD: Fistula complications (stenosis, thrombosis, infection, etc.) Dysequilibrium-syndrome at initiation (brain oedema with headache, confusion, coma) Fluid overload, but also dehydration Hyperkaliaemia Hepatitis B and C infection Kachexia PNP Psychological problems

19. ......questions? ....thank you!