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Acute Kidney Injury & Chronic Kidney Disease UofG Urology Society Reiss StoopsPart One – Acute Kidney Injury Definition Acute kidney injury (AKI) is defined as an abrupt deterioration in renal function, usually over hours or days, which is usually (but not always) reversible over days or weeks AKI is usually recognised with reduced urine output, rising serum urea and creatinine, or both (Many Guideline Definitions) AKI is frequently multifactorial Clinical Features The early stages of AKI are often completely asymptomatic. It is not the accumulation of urea itself that causes symptoms, but a combination of many different metabolic abnormalities Clinical Features 1. Alteration of Urine Volume: Oliguria usually occurs in the early stages. Patients are usually oliguric (urine volume < 500 mL daily). Recovery of renal function typically occurs after 7–21 days and in the recovery phase, which may last some weeks, there is often passage of large amounts of dilute urine. Clinical Features 2. Biochemical Abnormalities: AKIs can lead to: • Hyperkalaemia • Metabolic Acidosis • Hyponatraemia (water overload following oliguria) • Hypocalcaemia (reduced renal production of 1,25-D3) • Hyperphosphatemia (phosphate retention) Clinical Features 3. Uraemia: Uraemia = raised level serum urea that is normally excreted by kidneys Symptoms include weakness, fatigue, anorexia, nausea and vomiting, followed by mental confusion, seizures and coma. Breathlessness occurs from a combination of anaemia, acidosis and pulmonary oedema secondary to volume overload. Pathology Pathology of AKI categorised: 1. Pre-Renal 2. Renal 3. Post-Renal Pathology 1. Pre-Renal AKI • Hypovolaemia Reduced renal blood flow (Dehydration/Haemorrhage) = reduced GFR. Changes • Hypotension (Septic shock) in circulation or intrarenal changes that drop • Low Cardiac Output (heart glomerular perfusion failure) pressures • NSAIDs, ACE Inhibitors etc. Pathology 1. Pre-Renal AKI Pathology 2. Renal AKI Most commonly (80– 90%) due to acute tubular necrosis Others include: • Glomerulonephritis • Vasculitis • Pyelonephritis Pathology 3. Post-Renal AKI Obstruction of the urinary tract at any point from the calyces to the external urethral orifice Most common - bladder outflow obstruction (prostate disease) or ureteric obstruction (stones or tumours). Investigations • U&Es • FBC • CRP • Urine Dipstick and Microscopy (Glomerulonephritis if haematuria and proteinuria) • Urine & Blood Cultures • Renal USS (Obstruction & Tumour) • Urinary Electrolytes Management cause:ment of AKI requires correct diagnosis to treat underlying Pre-Renal – Volume correction, antibiotics, increase renal perfusion (cardiac support) Renal – Biopsy & Refer to specialist Post-Renal – Catheter, nephrostomy, stone removal, tumour resection, urological interventionPart Two – Chronic Kidney Disease Definition Chronic kidney disease (CKD) refers to an irreversible deterioration in renal function that classically develops over a period of years It is defined on the basis of persistent (> 3 months) evidence of kidney damage (proteinuria, haematuria, or anatomical abnormality) and/or impaired GFR When death is likely without renal replacement therapy, the condition is called end-stage renal disease (ESRD).CKD Stages Clinical Features Patients may remain asymptomatic until GFR falls < 30mL/min Main clinical features based on kidney dysfunction: 1. Anaemia (Reduced erythropoietin) 2. Bone Disease (Reduced 1-25-D3) – Osteoporosis, Osteopenia 3. Polyneuropathy (Uraemia) 4. Cardiovascular Disease – MI, H, Stroke – Increased BP 5. Immune Dysfunction 6. General – fatigue, breathlessness, metabolic acidosis, nausea Pathology CKD may be caused by any condition that destroys the normal structure and function of the kidney: • Diabetic Nephropathy • Interstitial & Glomerular Disease • Hypertension • Systemic Inflammatory Diseases • Renal Abnormalities / Developmental Defects • Polycystic Kidney Disease Investigations Initial screening tests in CKD are similar to AKI. The aims are to: • Identify the underlying cause •Address reversible factors that are making renal function worse, e.g. hypertension, urinary tract obstruction or infection, and nephrotoxic medications •Screen for complications such as osteodystrophy or anaemia • Screen for cardiovascular risk factors. Management The aims of treatment are: • Specific therapy for underlying cause of renal disease, e.g. diabetesppressive agents for vasculitis and tight control in • Slow deterioration of kidney function (renoprotection) • Reduce cardiovascular risk • Treat the complications, e.g. anaemia, acidosis, infections, electrolyte imbalances • Appropriate dose adjustment of prescribed drugs • Continuous Monitoring CKD vs AKI Distinction between AKI and CKD depends on: •History •Duration of symptoms •Previous urinalysis or measurement of serum creatinine A normochromic anaemia, small kidneys on USS and the presence of renal osteodystrophy favour a chronic process.Thank You! Questions