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Acute and chronic renal failure. Etiology, pathogenesis. Diagnostics. Clinical picture. Complications. Principles of treatment. The role of a doctor-dentist.

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Presentation on theme: "Acute and chronic renal failure. Etiology, pathogenesis. Diagnostics. Clinical picture. Complications. Principles of treatment. The role of a doctor-dentist."— Presentation transcript:

1 Acute and chronic renal failure. Etiology, pathogenesis. Diagnostics. Clinical picture. Complications. Principles of treatment. The role of a doctor-dentist in early diagnostics and prophylaxis.

2 Epidemiology Recent studies have found an overall incidence of acute kidney injury (AKI) of almost 500 per million per year and the incidence of AKI needing dialysis being more than 200 per million per year. Prerenal AKI and ischaemic acute tubular necrosis (ATN) together account for 75% of the cases of AKI.

3 Causes of acute kidney injury Prerenal:  Volume depletion (eg haemorrhage, severe vomiting or diarrhoea, burns, inappropriate diuresis)  Oedematous states: cardiac failure, cirrhosis, nephrotic syndrome  Hypotension (eg cardiogenic shock, sepsis, anaphylaxis)  Cardiovascular (eg severe cardiac failure, arrhythmias)  Renal hypoperfusion: non-steroidal anti-inflammatory drugs (NSAIDs) or selective cyclooxygenase-2 (COX-2) inhibitors, angiotensin-converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists, abdominal aortic aneurysm, renal artery stenosis or occlusion, hepatorenal syndrome

4 Intrinsic acute kidney injury (AKI):  Glomerular disease: glomerulonephritis, thrombosis, haemolytic uraemic syndrome  Tubular injury: acute tubular necrosis (ATN) following prolonged ischaemia; nephrotoxins (eg aminoglycosides, radiocontrast media, myoglobin, cisplatin, heavy metals, light chains in myeloma kidney)  Acute interstitial nephritis due to drugs (eg NSAIDs), infection or autoimmune diseases  Vascular disease: vasculitis (usually associated with antineutrophil cytoplasmic antibody), cryoglobulinaemia, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal artery stenosis, renal vein thrombosis, malignant hypertension  Eclampsia

5 Postrenal:  Calculus  Blood clot  Papillary necrosis  Urethral stricture  Prostatic hypertrophy or malignancy  Bladder tumour  Radiation fibrosis  Pelvic malignancy  Retroperitoneal fibrosis

6 Risk factors  People with the following comorbid conditions are at a higher risk for developing AKI:[2]  Elderly  Hypertension  Vascular disease  Pre-existing renal impairment  Congestive cardiac failure  Diabetes  Myeloma  Chronic infection  Myeloproliferative disorder

7 The presentation will depend on the underlying cause and severity of AKI. There may be no symptoms or signs, but oliguria (urine volume less than 400 mL/24 hours) is common. There is an accumulation of fluid and nitrogenous waste products demonstrated by a rise in blood urea and creatinine.

8 Signs  Hypertension  Abdomen: may reveal a large, painless bladder typical of chronic urinary retention  Dehydration with postural hypotension and no oedema  Fluid overload with raised JVP, pulmonary oedema and peripheral oedema  Pallor, rash, bruising: petechiae, purpura, and nosebleeds may suggest inflammatory or vascular disease, emboli or disseminated intravascular coagulation  Pericardial rub Symptoms  Urine output: AKI is usually accompanied by oliguria or anuria, but polyuria may occur.  Abrupt anuria suggests an acute obstruction, acute and severe glomerulonephritis, or acute renal artery occlusion.  Gradual diminution of urine output may indicate a urethral stricture or bladder outlet obstruction, eg benign prostatic hyperplasia.  Nausea, vomiting  Dehydration  Confusion

9  Factors that suggest CKD include long duration of symptoms, nocturia, absence of acute illness, anaemia, hyperphosphataemia, hypocalcaemia.  Previous creatinine measurements if available are very useful.  Reduced renal size and cortical thickness on ultrasound is characteristic of CKD (renal size is typically preserved in patients with diabetes). Distinguish acute and chronic kidney disease

10 Exclude urinary tract obstruction:  History of previous stones or symptoms of bladder outflow obstruction  Palpable bladder  Complete anuria suggests renal tract obstruction  Renal ultrasound is the best method to detect dilatation of the renal pelvis and calyces (obstruction may be present without dilatation, especially in patients with malignancy)

11 Evidence of renal parenchymal disease:  Features of underlying systemic disease, eg rashes, arthralgia, myalgia  Use of antibiotics and NSAIDs  Urine dipstick and microscopy: dipstick blood or protein, or dysmorphic red cells, red cell casts (suggestive of glomerulonephritis), or eosinophils (suggestive of acute interstitial nephritis) on microscopy

12 Differential diagnosis  Chronic kidney disease: factors that suggest CKD include:  Long duration of symptoms  Nocturia  Absence of acute illness  Anaemia  Hyperphosphataemia, hypocalcaemia (but similar laboratory findings may complicate acute kidney injury (AKI))  Reduced renal size and cortical thickness on renal ultrasound (but renal size is typically preserved in patients with diabetes

13 Investigations  Urinalysis:  Urinalysis: blood and/or protein suggests a renal inflammatory process; microscopy for cells, casts, crystals; red cell casts diagnostic in glomerulonephritis; tubular cells or casts suggest acute tubular necrosis (ATN)  Urine osmolality: osmolality of urine is over 500 mmol/kg if the cause is pre-renal and 300 mmol/kg or less if it is renal; patients with ATN lose the ability to concentrate and dilute the urine and will pass a constant volume with inappropriate osmolality  Biochemistry: Traditional blood (creatinine, blood urea nitrogen) and urine markers of kidney injury (epithelial cells, tubular casts, fractional excretion of Na+, urinary concentrating ability, etc.) are insensitive and nonspecific for the diagnosis of acute kidney injury (AKI). Work continues to find an appropriate biomarker, eg cystatin C (Cys-C).

14  Serial urea, creatinine, electrolytes: important metabolic consequences of AKI include hyperkalaemia, metabolic acidosis, hypocalcaemia, hyperphosphataemia (serum urea is a poor marker of renal function because it varies significantly with hydration diet, it is not produced constantly and it is reabsorbed by the kidney).  Serum creatinine has significant limitations. The level can remain within the normal range despite the loss of over 50% of renal function.  Creatine kinase, myoglobinuria: markedly elevated creatine kinase and myoglobinuria suggest rhabdomyolysis.  Haematology:  Full blood count, blood film: eosinophilia may be present in acute interstitial nephritis, cholesterol embolisation, or vasculitis; thrombocytopenia and red cell fragments suggest thrombotic microangiopathy.  Coagulation studies: disseminated intravascular coagulation associated with sepsis. Investigations

15 Immunology: Cys-C: over the past decade serum Cys-C has been extensively studied and found to be a sensitive serum marker of GFR and a stronger predictor than serum creatinine of risk of death and cardiovascular events in older patients. C reactive protein: nonspecific marker of infection or inflammation. Serum immunoglobulins, serum protein electrophoresis, Bence Jones' proteinuria: immune paresis, monoclonal band on serum protein electrophoresis, and Bence Jones' proteinuria suggest myeloma.

16 Antinuclear antibody (ANA): ANA positive in systemic lupus erythematosus (SLE) and other autoimmune disorders; anti-double stranded (anti-dsDNA) antibodies more specific for SLE; anti-dsDNA antibodies; antineutrophil cytoplasmic antibody (ANCA) (associated with systemic vasculitis; classical antineutrophil cytoplasmic antibodies (c-ANCA) and antiproteinase 3 (anti-PR3) antibodies associated with Wegener's granulomatosis; protoplasmic-staining antineutrophil cytoplasmic antibodies (p-ANCA) and antimyeloperoxidase (anti-MPO) antibodies present in microscopic polyangiitis), anti-PR3 antibodies, anti-MPO antibodies.

17 Complement concentrations: low in SLE, acute postinfectious glomerulonephritis, cryoglobulinaemia. Antiglomerular basement membrane (anti-GBM) antibodies: present in Goodpasture's disease. Antistreptolysin O and anti-DNAse B titres: high after streptococcal infection. Virology: Hepatitis B and C; HIV: important implications for infection control within dialysis area

18 Radiology: Renal ultrasonography: renal size, symmetry, evidence of obstruction Chest X-ray (pulmonary oedema); abdominal X-ray if renal calculi are suspected Contrast studies such as intravenous urogram (IVU) and renal angiography should be avoided because of the risk of contrast nephropathy Doppler ultrasound of the renal artery and veins: assessment of possible occlusion of the renal artery and veins Magnetic resonance angiography: for more accurate assessment of renal vascular occlusion ECG: recent myocardial infarction, tented T waves in hyperkalaemia Renal biopsy

19 Principles of management of acute kidney injury  No drug treatment has been shown to limit the progression of, or speed up recovery from, AKI.  Identify and correct prerenal and postrenal factors.  Optimise cardiac output and renal blood flow.  Review drugs: stop nephrotoxic agents; adjust doses and monitor concentrations where appropriate.  Accurately monitor fluid balance and daily body weight.  Identify and treat acute complications (hyperkalaemia, acidosis, pulmonary oedema).  Optimise nutritional support: adequate calories, minimal nitrogenous waste production, potassium restriction.  Identify and aggressively treat infection; minimise indwelling lines; remove bladder catheter if anuric.  Identify and treat bleeding tendency: prophylaxis with proton pump inhibitor (PPI) or h2-receptor antagonist (H2RA), transfuse if required, avoid aspirin.

20 Principles of management of acute kidney injury  Accurate control of fluid balance (avoid volume overload or depletion)  Daily measurement of serum electrolytes, potassium and sodium restriction, nutritional support  Prevention of gastrointestinal haemorrhage  Careful drug dosing and avoidance of nephrotoxic drugs  Specific treatment of underlying intrinsic renal disease where appropriate  Dialysis or haemofiltration Complications Life-threatening complications include:  Volume overload (severe pulmonary oedema)  Hyperkalaemia  Metabolic acidosis  Spontaneous haemorrhage, eg gastrointestinal

21 The definition of chronic kidney disease (CKD) is based on the presence of kidney damage (ie albuminuria) or decreased kidney function (ie glomerular filtration rate (GFR) <60 ml/minute per 1·73 m²) for three months or more, irrespective of clinical diagnosis.

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23 A large primary care study (practice population 162,113) suggests an age standardised prevalence of stage 3-5 chronic kidney disease (CKD) of 8.5% (10.6% in females and 5.8% in males).

24 Chronic renal failure (CRF) is characterized by progressive destruction of renal mass with irreversible sclerosis and loss of nephrons over a period of at least months to many years, depending on the underlying etiology. Glomerular filtration rate (GFR) progressively decreases with nephron loss, and the term CRF should be reserved more specifically for patients whose GFR is less than 30 cc/min.

25 Arteriopathic renal disease. Hypertension. Glomerulonephritis. Diabetes. Infective, obstructive and reflux nephropathies. Family history of stage 5 CKD or hereditary kidney disease Hypercalcaemia. Multisystem diseases with potential kidney involvement. Neoplasms. Myeloma. Aetiology In developed countries, CKD is often associated with old age, diabetes, hypertension, obesity and cardiovascular disease (CVD).

26 Risk factors  Factors other than the underlying disease process that may cause progressive renal injury include the following:  Acute insults from nephrotoxins or decreased perfusion.  Proteinuria.  Increased renal ammonia formation with interstitial injury.  Hyperlipidaemia.  Hyperphosphataemia with calcium phosphate deposition.

27 Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: Systemic hypertension Acute insults from nephrotoxins or decreased perfusion Proteinuria Increased renal ammoniagenesis with interstitial injury Hyperlipidemia Hyperphosphatemia with calcium phosphate deposition Decreased levels of nitrous oxide

28 Classification of chronic kidney disease  Kidney function should be assessed by eGFR and CKD is classified on this basis:[2]  Stage 1: normal; eGFR >90 ml/minute/1.73 m2 with other evidence of chronic kidney damage (see below).  Stage 2: mild impairment; eGFR ml/minute/1.73 m2 with other evidence of chronic kidney damage.  Stage 3a: moderate impairment; eGFR ml/minute/1.73 m2.  Stage 3b: moderate impairment; eGFR ml/minute/1.73 m2.  Stage 4: severe impairment; eGFR ml/minute/1.73 m2.  Stage 5: established renal failure (ERF); eGFR less than 15 ml/minute/1.73 m2 or on dialysis.

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30 Use the suffix (p) to denote the presence of proteinuria when staging CKD. NB: patients with a GFR of >60 ml/minute/1.73 m2 without evidence of chronic kidney damage should NOT be considered to have CKD and do not necessarily need further investigation.

31 The other evidence of chronic kidney damage may be one of the following:  Persistent microalbuminuria.  Persistent proteinuria.  Persistent haematuria (after exclusion of other causes - eg, urological disease).  Structural abnormalities of the kidneys, demonstrated on ultrasound scanning or other radiological tests - eg, polycystic kidney disease, reflux nephropathy.  Biopsy-proven chronic glomerulonephritis.

32 Symptoms  it usually presents with nonspecific symptoms caused by renal failure, complications - eg, anaemia in chronic renal failure (CRF), and the underlying disease.  It may be discovered by chance following a routine blood or urine test.  Specific symptoms usually develop only in severe renal failure, and include anorexia, nausea, vomiting, fatigue, weakness, pruritus, lethargy, peripheral oedema, dyspnoea, insomnia, muscle cramps, pulmonary oedema, nocturia, polyuria and headache.  Sexual dysfunction is common.  Hiccups, pericarditis, coma and seizures are only seen in very severe renal failure.

33 Signs of CKD include increased skin pigmentation or excoriation, pallor, hypertension, postural hypotension, peripheral oedema, left ventricular hypertrophy, peripheral vascular disease, pleural effusions, peripheral neuropathy and restless legs syndrome. Signs The physical examination is often not very helpful but may reveal findings characteristic of the underlying cause (eg SLE, severe arteriosclerosis, hypertension) or complications of CRF (eg, anaemia, bleeding diathesis, pericarditis).

34 Differential diagnosis Acute kidney injury (acute renal failure):  Making the distinction between AKI and CRF can be very difficult. A history of chronic symptoms of fatigue, weight loss, anorexia, nicturia, and pruritus all suggest CKD.  The history and examination will provide clues, but renal ultrasound will provide the most important information. Renal abnormalities on ultrasound, such as small kidneys in chronic glomerulonephritis or large cystic kidneys in adult polycystic kidney disease, will almost always be present in patients with CKD.  Acute on chronic renal failure: may have features indicating CKD but also features suggesting a cause of an acute deterioration of renal function - eg, infection.

35 Serum creatinine also has significant limitations. The level can remain within the normal range despite the loss of over 50% of renal function. A gold-standard measurement is an isotopic GFR, but this is expensive and not widely available. For most purposes in primary care, the best assessment or screening tool is the eGFR.[5] - see separate article Assessing Renal Function and the Estimated Glomerular Filtration Rate Calculator. Most laboratories now provide an eGFR when requesting serum creatinine, which should be used in preference to calculator above. Investigations Investigations are focused on assessment of renal function and therefore stage of CKD, identification of the underlying cause and assessment of complications of CKD.[1] Assessment of renal function: Serum urea is a poor marker of renal function, because it varies significantly with hydration and diet, is not produced constantly and is reabsorbed by the kidney.

36 Biochemistry: Plasma glucose: to detect undiagnosed diabetes or assess control of diabetes. Serum sodium: usually normal, but may be low. Serum potassium: raised. Serum bicarbonate: low. Serum albumin: hypoalbuminaemia in patients who are nephrotic and/or malnourished (low levels at the start of dialysis are associated with a poor prognosis). Serum calcium: may be normal, low or high. Serum phosphate: usually high. Serum alkaline phosphatase: raised when bone disease develops. Serum parathyroid hormone: rises progressively with declining renal function. Serum cholesterol and triglycerides: dyslipidaemia is common.

37 Hepatitis serology: ensure not infected and vaccinate against hepatitis B. HIV serology: performed before dialysis or transplantation. Haematology: Normochromic normocytic anaemia; haemoglobin falls with progressive renal failure. White cells and platelets are usually normal. Serology: Autoantibodies, particularly antinuclear antibodies, classical antineutrophil cytoplasmic antibodies (c-ANCA), protoplasmic- staining antineutrophil cytoplasmic antibodies (p-ANCA), antiglomerular basement membrane (anti-GBM) antibodies (very suggestive of underlying Goodpasture's syndrome) and serum complement.

38 Urine: Urinalysis: dipstick proteinuria may suggest glomerular or tubulointerstitial disease. Urine sediment with red blood cells and red blood cell casts suggests proliferative glomerulonephritis. Pyuria and/or white cell casts suggest interstitial nephritis (especially if eosinophils are present in the urine) or urinary tract infection (UTI). Spot urine collection for total protein:creatinine ratio allows reliable estimation of total 24-hour urinary protein excretion. The degree of proteinuria correlates with the rate of progression of the underlying kidney disease and is the most reliable prognostic factor in CKD. 24-hour urine collection for total protein and creatinine clearance. To detect and identify proteinuria, use urine albumin:creatinine ratio (ACR) in preference, as it has greater sensitivity than protein:creatinine ratio (PCR) for low levels of proteinuria. For quantification and monitoring of proteinuria, PCR can be used as an alternative. ACR is the recommended method for people with diabetes.

39 Patients in whom initial urinalysis reveals microscopic haematuria should have a urine culture performed to exclude a UTI. If a UTI is excluded, two further tests should be performed to confirm the presence of persistent microscopic haematuria.[6] Patients over 40 years of age with persistent non-visible/microscopic haematuria in the absence of significant proteinuria or a reduced GFR should be referred to a urology department for further investigation.[6] Serum and urine protein electrophoresis: to screen for a monoclonal protein possibly representing multiple myeloma.

40 ECG and echocardiography: to detect left ventricular hypertrophy and ischaemia, and to assess cardiac function. Imaging of the renal tract: Plain abdominal X-ray: may show radio-opaque stones or nephrocalcinosis. Intravenous (IV) pyelogram: not often used because of potential for contrast nephropathy.

41 In newly diagnosed with eGFR less than 60 ml/minute/1.73 m2 Review all previous measurements of serum creatinine to estimate GFR and assess the rate of deterioration. Review all medication including over-the- counter drugs; particularly consider recent additions (eg, diuretics, NSAIDs, or any drug capable of causing interstitial nephritis, such as penicillins, cephalosporins, mesalazine). Urinalysis: haematuria and proteinuria suggest glomerulonephritis, which may progress rapidly. Clinical assessment: eg, look for sepsis, heart failure, hypovolaemia, palpable bladder. Repeat serum creatinine measurement within five days to exclude rapid progression. Check criteria for referral (above). If referral is not indicated, ensure entry into a chronic disease management register and programme.

42 Renal ultrasound:  Small echogenic kidneys are seen in advanced renal failure.  Kidneys are usually initially large and then become normal in size in advanced diabetic nephropathy.  Structural abnormalities may be seen - eg, polycystic kidneys.  It is also used to screen for hydronephrosis caused by urinary tract obstruction, or involvement of the retroperitoneum with fibrosis, tumour or diffuse adenopathy.  Retrograde pyelogram: may be indicated if there is clinical suspicion of obstruction despite a negative ultrasound study finding.  Renal radionuclide scan:  Useful to screen for renal artery stenosis when performed with captopril administration but is unreliable for GFR of less than 30 ml/minute.  Also quantifies differential renal contribution to total GFR.

43  CT scan: to define renal masses and cysts, seen on ultrasound, better; this is the most sensitive test for identifying renal stones.  MRI:  For patients who require a CT scan but who cannot receive IV contrast.  Like CT scan and renal venography, it is reliable in the diagnosis of renal vein thrombosis.  Magnetic resonance angiography is also useful for diagnosis of renal artery stenosis, although renal arteriography remains the investigation of choice.  Micturating cystourethrogram: for diagnosis of vesicoureteric reflux.  Renal biopsy.

44 Complications  Anaemia: left ventricular hypertrophy, fatigue, impaired cognitive functioning.  Coagulopathy.  Hypertension: left ventricular hypertrophy, heart failure, stroke, CVD.  Calcium phosphate loading: cardiovascular and cerebrovascular disease, arthropathy, soft tissue calcification.  Renal osteodystrophy: disorders of calcium, phosphorus and bone, most commonly osteitis fibrosa cystica.  Bone changes of secondary hyperparathyroidism: bone pain and fractures.  Neurological: uraemic encephalopathy, neuropathy including peripheral neuropathy.  Dialysis amyloid: bone pain, arthropathy, carpal tunnel syndrome.  Fluid overload: pulmonary oedema, hypertension  Malnutrition: increased morbidity and mortality, infections, poor wound healing.  Glucose intolerance due to peripheral insulin resistance.

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46 When symptoms are severe they can be treated only by dialysis and transplantation (end-stage renal disease). Kidney failure is defined as a GFR of less than 15 ml/minute per 1·73 m², or the need for treatment with dialysis or transplantation

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48 Prognosis Early diagnosis, regular monitoring and early treatment can prevent development and slow disease progression, reduce complications and the risk of cardiovascular disease, and improve survival and quality of life.[1] Much of the damage caused by CKD occurs early, when interventions may be much more effective. Rapidly progressive diseases can lead to kidney failure within months. However, most diseases evolve over decades and some patients do not progress during many years of follow-up.[1] Patients on chronic dialysis have a high incidence of morbidity and mortality. Patients with end-stage renal disease (ESRD) who undergo renal transplantation survive longer than those on chronic dialysis. CVD is the most common cause of death in patients with CKD. Cardiovascular mortality is doubled in patients with a GFR below 70 ml/minute.

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