Acute kidney injury Acute kidney injury AKI previously referred to as acute renal failure is not a diagnosis rather it describes the situation where there is a sudden and often reversible loss of renal function ID: 1032995
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1. Renal Failure Dr MARWAN MAJEED IBRAHIM
2. Acute kidney injuryAcute kidney injury (AKI), previously referred to as acute renal failure, is not a diagnosis; rather it describes the situation where there is a sudden and often reversible loss of renal function, which develops over days or weeks and is often accompanied by a reduction in urine volume. In uncomplicated AKI mortality is low, even when RRT is required. In AKI associated with sepsis and multiple organ failure, mortality is 50–70% and the outcome is usually determined by the severity of the underlying disorder and other complications, rather than by kidney injury itself.
3. Pathophysiology There are many causes of AKI and it is frequently multifactorial. It is helpful to classify it into three subtypes: • ‘pre-renal’, when perfusion to the kidney is reduced • ‘renal’, when the primary insult affects the kidney itself • ‘post-renal’, when there is obstruction to urine flow at any point from the tubule to the urethra. In pre-renal AKI, a reduction in perfusion reduces GFR. If the insult is not corrected, this may lead to ‘renal’ injury: namely, acute tubular necrosis (ATN).
4. Renal AKI may be caused by nephrotoxic drugs, which can cause ATN or allergic interstitial nephritis. The other common ‘renal’ cause is glomerulonephritis, in which there is direct inflammatory damage to the glomeruli.Post-renal AKI occurs as the result of obstruction to the renal tract. This leads to elevation of intraluminal ureteral pressure transmitted to the nephrons after prolonged obstruction, with a subsequent fall in GFR. This leads to chronic renal injury over time (several weeks). Recovery of renal function depends on the duration of obstruction and the pre-morbid GFR.
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8. ManagementHemodynamic status : If hypovolemia is present, it should be corrected by replacement of intravenous fluid or blood; excessive administration of fluid should be avoided, since this can provoke pulmonary oedema and worsen outcome in AKI. Monitoring of central venous pressure may be of value in determining the rate of administration of fluid in these circumstances. Balanced crystalloid solutions, such as Plasma-Lyte, Hartmann’s or Ringer’s lactate, may be preferable to isotonic saline (0.9% NaCl) when large volumes of fluid resuscitation are required, in order to avoid hyperchloremic acidosis, but whether this substantially influences outcome remains unclear.
9. Hyperkalaemia: is common, particularly in patients with rhabdomyolysis, burns, hemolysis or metabolic acidosis serum K+ concentration is > 6.5 mmol/L, this should be treated immediately, to prevent life-threatening cardiac arrhythmias. Metabolic acidosis: develops unless prevented by loss of hydrogen ions through vomiting. Severe acidosis can be ameliorated with sodium bicarbonate if volume status allows. Restoration of blood volume will correct acidosis by restoring kidney function. Infusions of isotonic sodium bicarbonate may also be used, if acidosis is severe, to reduce life-threatening hyperkaliemia
10. Cardiopulmonary complications: Pulmonary oedema may be caused by the administration of excessive amounts of fluids relative to urine output and by increased pulmonary capillary permeability. If pulmonary edema is present and urine output cannot be rapidly restored, treatment with dialysis may be required to remove excess fluid. Once initial resuscitation has been performed, fluid intake should be matched to urine output plus 500 mL per day to cover insensible losses, unless diarrhea is present, in which case additional fluids may be required.
11. Medications Patients with drug-induced kidney injury should have the offending drug withdrawn. Additionally, vasoactive medications, such as NSAIDs and ACE inhibitors, should be discontinued, as they may prolong AKI. H2-receptor antagonists or PPIs should be given to prevent gastrointestinal bleeding.
12. Renal tract obstruction In post-renal AKI, the obstruction should be relieved as soon as possible. This may involve urinary catheterization for bladder outflow obstruction, or correction of ureteric obstruction with a ureteric stent or percutaneous nephrostomy.
13. Renal replacement therapy Conservative management can be successful in AKI with meticulous attention to fluid balance, electrolytes and nutrition, but RRT may be required in patients who are not showing signs of recovery with these measures. No specific cut-off values for serum urea or creatinine have been identified at which RRT should be commenced. The two main options for RRT in AKI are intermittent haemodialysis and CRRT. Peritoneal dialysis is also an option if haemodialysis is not available
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17. Chronic kidney diseaseChronic kidney disease (CKD) refers to an irreversible deterioration in renal function that usually develops over a period of yearsWhen death is likely without RRT (CKD stage 5), it is called end-stage renal disease (ESRD).
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19. Clinical features The typical presentation is for a raised urea and creatinine to be found incidentally during routine blood tests, often during screening of high-risk patients, such as those with diabetes or hypertension. Most patients with slowly progressive disease are asymptomatic until GFR falls below 30 mL/min/1.73 m2 and some can remain asymptomatic with much lower GFR values than this. An early symptom is nocturia, due to the loss of concentrating ability and increased osmotic load per nephron, but this is non-specific. When GFR falls below 15–20 mL/min/1.73 m2, symptoms and signs are common and can affect almost all body systems.
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22. They typically include tiredness or breathlessness, which may, in part, be related to renal anemia or fluid overload. With further deterioration in renal function, patients may suffer pruritus, anorexia, weight loss, nausea, vomiting and hiccups. In very advanced renal failure, respiration may be particularly deep (Kussmaul breathing) due to profound metabolic acidosis, and patients may develop muscular twitching, fits, drowsiness and coma.
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24. ManagementMonitoring of renal functionThe rate of change in renal function varies between patients and may vary over time in each individual. Renal function should therefore be monitored every 6 months in patients with stage 3 CKD, but more frequently in patients who are deteriorating rapidly or have stage 4 or 5 CKD.
25. Antihypertensive therapy: Lowering of blood pressure slows the rate at which renal function declines in CKD, lowering the risk of hypertensive heart failure, stroke and peripheral vascular diseaseVarious targets have been suggested, such as 140/90 mmHg for patients with CKD and no albuminuria (ACR < 3 mg/mmol). A lower target of 130/80 mmHg should be considered for those who have moderately elevated albuminuria (ACR 3 mg/mmol), and is recommended for those with an ACR of more than 30 mg/mmol. Even lower targets, such as 125/75 mmHg, may be prudent in patients with CKD and heavy proteinuria (ACR > 70 mg/ mmol).
26. ACE inhibitors and ARBs reduce proteinuria and retard the progression of CKD.ACE inhibitors and/or ARBs should be prescribed to all patients with diabetic nephropathy and patients with CKD and proteinuria, irrespective of whether or not hypertension is present.
27. Treatment of complicationsPotassium intake to below 70 mmol Potassium binding compounds limit absorption of potassium from the gut and may be a useful adjunctive therapy.Patients with evidence of volume expansion should be instructed to consume a low-sodium diet (< 100 mmol/24 hrs.), and in severe cases fluid intake should also be restricted. Diuretics are commonly required, and as renal function deteriorates, increasing doses of potent loop diuretics or synergistic combinations of loop, thiazide and potassium-sparing diuretics may be necessary.
28. Acid–base balance: Reduced ability to excrete organic acids in patients with CKD may lead to an anion-gap metabolic acidosisPlasma bicarbonate concentrations should be maintained above 22 mmol/L by prescribing sodium bicarbonate supplements.
29. Renal bone disease Disturbances of calcium and phosphate metabolism are almost universal in advanced CKD The sequence of events that leads to renal bone disease is complex, but two primary factors are impaired excretion of phosphate and failure of the renal tubular cells to convert 25-hydroxyvitamin D to its active metabolite, 1,25-dihydroxyvitamin D.
30. Both the reduced absorption and increased deposition of calcium cause hypocalcemia, which also stimulates PTH production by the parathyroid glands. Hence in many patients with CKD, compensatory responses initially maintain phosphate and calcium levels at the upper and lower ends of their respective normal ranges, at the expense of an elevated PTH level (secondary hyperparathyroidism). This is associated with a gradual transfer of calcium and phosphate from the bone to other tissues, leading to bone resorption (osteitis fibrosa cystica), and in severe cases this may result in bony pain and increased risk of fractures
31. In some cases, tertiary hyperparathyroidism supervenes, due to autonomous production of PTH by the enlarged parathyroid glands; this presents with hypercalcemia. Additional problems in bone metabolism include low bone turnover (adynamic bone disease) in patients who have been over-treated with vitamin D metabolites, osteomalacia with over-treatment of hyperphosphatasemia, and osteoporosis in patients with poor nutritional intake.
32. The key focus in the management of renal bone disease should be directed towards the two main driving factors, hyperphosphataemia and inadequate activation of vitamin DHyperphosphataemia should be treated by dietary restriction of foods with high phosphate content (milk, cheese, eggs and protein-rich foods) and by the use of phosphate-binding drugs. Various drugs are available, including calcium carbonate, aluminium hydroxide, lanthanum carbonate and polymer-based phosphate binders such as sevelamer. The aim is to maintain serum phosphate values at or below 1.5 mmol/L (4.6 mg/dL) if possible, but many of these drugs are difficult to take and adherence can be a problem.
33. Active vitamin D metabolites (either 1-α-hydroxyvitamin D or 1,25-dihydroxyvitamin D) should be administered in patients who are hypocalcaemic or have serum PTH levels more than twice the upper limit of normal. The dose should be adjusted to try to reduce PTH levels to between 2 and 4 times the upper limit of normal to limit hyperparathyroidism while avoiding over-suppression of bone turnover and adynamic bone disease, but care must be exercised in order to avoid hypercalcemia.
34. Anaemia Anaemia is common in patients with CKD and contributes to many of the non-specific symptoms, including fatigue and shortness of breath. Hemoglobin can be as low as 50–70 g/L in CKD stage 5, although it is often less severe or absent in patients with polycystic kidney disease. Iron deficiency is common in patients with CKD, and even more prevalent in those on hemodialysis as a result of hemolysis in the dialysis circuit. Hence many patients require iron supplements, which may be given intravenously for those with iron intolerance or in situations where adherence may be difficult.
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36. Once iron deficiency and other causes of anaemia have been excluded or corrected, recombinant human erythropoietin is very effective in correcting the anaemia of CKD and improving symptoms. Erythropoietin treatment does not influence mortality, however, and correcting haemoglobin to normal levels may carry some extra risk, including hypertension and thrombosis. The target haemoglobin is usually between 100 and 120 g/L. Erythropoietin is less effective in the presence of iron deficiency, active inflammation or malignancy, in particular myeloma.
37. Renal replacement therapyHemodialysis Hemodialysis is the most common form of RRT in ESRD and is also used in AKI. Hemodialysis involves gaining access to the circulation, either through a central venous catheter or an arteriovenous fistula or graft.Hemofiltration This technique is principally used in the treatment of AKI as CRRT. Large volumes of water are filtered from blood across a porous semipermeable membrane under a pressure gradient. Solutes are removed via ‘solvent drag’.
38. Peritoneal dialysis Peritoneal dialysis is principally used in the treatment of CKD, though it may occasionally be employed in AKI. It requires the insertion of a permanent Silastic catheter into the peritoneal cavity
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40. Renal transplantation offers the best chance of long-term survival in ESRD and is the most cost-effective treatment. All patients with ESRD should be considered for transplantation but many are not suitable due to a combination of comorbidity and advanced age (although no absolute age limit applies). Active malignancy, vasculitis, cardiovascular disease and a high risk of recurrence of renal disease (generally glomerulonephritides) are common contraindications to transplantation.
41. transplant patients require regular life-long follow-up to monitor renal function and complications of immunosuppression.A common regimen is triple therapy with prednisolone; ciclosporin or tacrolimus; and azathioprine or mycophenolate mofetil. Sirolimus is an alternative that can be introduced laterThe prognosis after kidney transplantation is good.
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