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. Epidemiology
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.
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.
PrerenalAKI and ischaemic acute tubular necrosis (ATN) together account for 75% of the cases of AKI.
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.
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.
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.
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.
Hepatitis B and C; HIV: important implications for infection control within dialysis area
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
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.
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).
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.
In developed countries, CKD is often associated with old age, diabetes, hypertension, obesity and cardiovascular disease (CVD).
Infective, obstructive and reflux nephropathies.
Family history of stage 5 CKD or hereditary kidney disease
Multisystem diseases with potential kidney involvement.
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
• Increased renal ammoniagenesis with interstitial injury
• Hyperphosphatemia with calcium phosphate deposition
• Decreased levels of nitrous oxide
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.
The other evidence of chronic kidney damage may be one of the following:
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).
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.
Investigations are focused on assessment of renal function and therefore stage of CKD, identification of the underlying cause and assessment of complications of CKD.
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.
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. - 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.
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.
Normochromic normocytic anaemia; haemoglobin falls with progressive renal failure.
White cells and platelets are usually normal.
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.
Hepatitis serology: ensure not infected and vaccinate against hepatitis B.
HIV serology: performed before dialysis or transplantation.
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.
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.
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.
Serum and urine protein electrophoresis: to screen for a monoclonal protein possibly representing multiple myeloma.
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.
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.
CT scan: to define renal masses and cysts, seen on ultrasound, better; this is the most sensitive test for identifying renal stones.
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
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.
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.
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.