Acute kidney injury
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acute kidney injury

acute kidney injury
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  • occurring in young, otherwise healthy people, secondary to tropical infections, more severe in nature
  • In view of above problems, there was a need to develop reliable biomarkers particularly for AKI, akin to troponin for acute coronary syndrome.
  • Based on experimental models of AKI, a number of biomarkers have been proposed: • Cystatin C • Neutrophilgelatinase-associated lipocalin (NGAL) • Interleukin-18 • Kidney injury molecule-1 • N-acetyl-D-glucosaminidase.
  • ROLE OF BIOMARKERS Early detection of AKI The treatment of AKI ideally should begin before the diagnosis is firmly established. A high index of suspicion often is necessary to diagnose early AKI. The determination of Serum creatinine and FENa using spot urine remains the primary and most readily available early marker of AKI. Serum creatinine : Serum creatinine and urine output are still considered as the best existing, most widely used .easily available and cheap markers to diagnose AKI in its relatively early stages.. Fractional excretion of sodium (FeNa): Increase in FeNa is noted , even before oliguric phase is established and patient is still in potentially reversible phase of AKI. Cystatin-C Cystatin-C is an endogenous cysteineproteinase inhibitor of low molecular weight. Cystatin-C, is neither secreted nor reabsorbed but completely metabolized, by proximal renal tubular cells, unaffected by sex, age, height, weight, and muscle mass. Serum cystatin C, has been shown superior to serum creatinine, as a surrogate marker of early and subtle changes of kidney function. It identifies kidney injury while creatinine levels remain in the normal range and allow detection of AKI, 24-48 hours earlier than serum creatinine 25-26 Kidney Injury Molecule-1(KIM-1) KIM-1 is a type 1 trans-membrane served as a marker of severity of AKI and can be used to predict adverse outcomes in hospitalized patients better than conventionally used severity markers27-28.
  • The sparse controlled data available have shown that 250ml of mannitol 20% given immediately before vessel clamp removal reduces the inci- dence of post-transplant AKI, as indicated by a lower require- ment of post-transplant dialysis. However, 3 months after transplantation, no difference is found in kidney function compared to patients who did not receive mannitol.It has also been suggested that mannitol is beneficial in rhabdomyolysis by stimulating osmotic diuresis and by lowering the intracompartmental pressure in the affected crushed limbs
  • Its use has been abandoned by most. KDIGO recommend not using low-dose dopamine to prevent or treat AKI. (1A) Similarly, although there were trends towards transiently greater urine output, lower SCr, and higher GFR in dopamine-treated patients on day 1 of therapy (but not days 2 and 3), there was no evidence of a sustained beneficial effect on renal function.
  • FLUIDSIn the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. It is acknowledged that colloids may be chosen in some patients to aid in reaching resuscitation goals, or to avoid excessive fluid administration in patients requiring large volume resuscitation, or in specific patient subsets (e.g., a cirrhotic patient with spontaneous peritonitis, or in burns). Colloids- albumin displaying renoprotection and hyperoncotic starch showing nephro- toxicity.Excessive chloride administration from 0.9% saline may lead to hyperchloremic metabolic acidosis
  • The Work Group concluded that current clinical data are insufficient to conclude that one vasoactive agent is superior to another in preventing AKI, but emphasized that vasoactive agents should not be withheld from patients with vasomotor shock over concern for kidney perfusion. Indeed, appropriate use of vasoactive agents can improve kidney perfusion in volume-resuscitated patients with vasomotor shock.
  • However, with multiple negative studies, including a randomized, double-blind, placebo-controlled trial of adequate size and power, its use has been abandoned by most. Low-dose dopamine administration (1–3mg/kg/min) to healthy individuals causes renal vasodila- tion, natriuresis, and increased GFR; because of these effects, it has been given as prophylaxis for AKI associated with radiocontrast administration, repair of aortic aneurysms, orthotopic liver transplantation, unilateral nephrectomy, renal transplantation, and chemotherapy with interferon. However, with multiple negative studies, including a randomized, double-blind, placebo-controlled trial of adequate size and power,207 its use has been abandoned by most. Low-dose dopamine administration (1–3mg/kg/min) to healthy individuals causes renal vasodila- tion, natriuresis, and increased GFR; because of these effects, it has been given as prophylaxis for AKI associated with radiocontrast administration, repair of aortic aneurysms, orthotopic liver transplantation, unilateral nephrectomy, renal transplantation, and chemotherapy with interferon. We recommend not using low-dose dopamine to prevent or treat AKI. (1A) Similarly, although there were trends towards transiently greater urine output, lower SCr, and higher GFR in dopamine-treated patients on day 1 of therapy (but not days 2 and 3), there was no evidence of a sustained beneficial effect on renal function. These analyses found no evidence that dopamine therapy is effective in the prevention or treatment of AKI.
  • In addition, oliguric AKI has a worse prognosis than nonoliguric AKI and physicians often prescribe diuretics to convert oliguric to nonoliguric AKI. Furthermore, several diuretics have potentially renoprotective effects that might prevent development of AKI and hasten its recovery. However, diuretics can also be harmful, by reducing the circulating volume excessively and adding a prerenal insult, worsening established AKI.We recommend not using diuretics to prevent AKI. (1B) 3.4.2: We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C)Loop diuretics have several effects that may protect against AKI. They may decrease oxygen consumption in the loop of Henle by inhibiting sodium transport, thus potentially lessening ischemic injury. Na-K-2Cl cotransporter,184,185 resulting in a loss of the high medullaryosmolality and decreased ability to reabsorb water.Furosemide also might hasten recovery of AKI by washing out necrotic debris blocking tubules, and by inhibiting prostaglandin dehydro- genase, which reduces renovascular resistance and increases renal blood flow. Specifically, prophylactic furosemide was found to be ineffective or harmful when used to prevent AKI after cardiac surgery,189,190 and to increase the risk of AKI when given to prevent CI-AKI. Finally, furosemide therapy was also ineffective and possibly harmful when used to treat AKI. There is no evidence that the use of diuretics reduces the incidence or severity of AKI. Ho et al.192,193 conducted two comprehensive systematic reviews on the use of the loop diuretic frusemide (furosemide) to prevent or treat AKI. Furosemide may, however, be useful in achieving fluid balance to facilitate mechanical ventilation according to the lung-protective ventilation strategy in hemodynamically stable patients with acute lung injury We similarlyconclude that there is no evidence that the use of loop diuretics reduces the severity of AKI, or improves outcomes in this syndrome. Although the use of loop diuretics in early or established AKI facilitates management of fluid balance, hyperkalemia, and hypercalcemia, and is indicated for these clinical purposes, any putative role in the prevention or amelioration of AKI course is unproven.Thus, a beneficial role for loop diuretics in facilitating discontinuation of RRT in AKI is not evident.In addition, oliguric AKI has a worse prognosis than nonoliguric AKI and physicians often prescribe diuretics to convert oliguric to nonoliguric AKI. Furthermore, several diuretics have potentially renoprotective effects that might prevent development of AKI and hasten its recovery. However, diuretics can also be harmful, by reducing the circulating volume excessively and adding a prerenal insult, worsening established AKI.We recommend not using diuretics to prevent AKI. (1B) 3.4.2: We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C)Loop diuretics have several effects that may protect against AKI. They may decrease oxygen consumption in the loop of Henle by inhibiting sodium transport, thus potentially lessening ischemic injury. Na-K-2Cl cotransporter,184,185 resulting in a loss of the high medullaryosmolality and decreased ability to reabsorb water.Furosemide also might hasten recovery of AKI by washing out necrotic debris blocking tubules, and by inhibiting prostaglandin dehydro- genase, which reduces renovascular resistance and increases renal blood flow. Specifically, prophylactic furosemide was found to be ineffective or harmful when used to prevent AKI after cardiac surgery,189,190 and to increase the risk of AKI when given to prevent CI-AKI. Finally, furosemide therapy was also ineffective and possibly harmful when used to treat AKI. There is no evidence that the use of diuretics reduces the incidence or severity of AKI. Ho et al.192,193 conducted two comprehensive systematic reviews on the use of the loop diuretic frusemide (furosemide) to prevent or treat AKI. Furosemide may, however, be useful in achieving fluid balance to facilitate mechanical ventilation according to the lung-protective ventilation strategy in hemodynamically stable patients with acute lung injury We similarlyconclude that there is no evidence that the use of loop diuretics reduces the severity of AKI, or improves outcomes in this syndrome. Although the use of loop diuretics in early or established AKI facilitates management of fluid balance, hyperkalemia, and hypercalcemia, and is indicated for these clinical purposes, any putative role in the prevention or amelioration of AKI course is unproven.Thus, a beneficial role for loop diuretics in facilitating discontinuation of RRT in AKI is not evident.
  • We suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephro- toxic, therapeutic alternatives are available. The risk of AKI attributable to aminoglycosides is sufficiently high (up to 25% in some series, depending upon the definition of AKI used and thepopulation studied) The intrinsic risk of AKI with the administration of aminoglycosides has led some authors to recommend the elimination of aminoglycosides as a clinical treatment option.277 Certainly their use should be restricted to treat severe infections where aminoglycosides are the best, or only, therapeutic option. Repeated administration of aminoglycosides over several days or weeks can result in accumulation of aminoglycosides within the renal interstitium and within the tubular epithelial cells. This can result in a higher incidence of nephrotoxicity with repeated exposure to aminoglycosides over time. Older patients (465 years), patients with pre-existing renal dysfunction, and septic patients with intravascular volume depletion and rapid alterations in fluid dynamics may be at greater risk for aminoglycosidenephrotoxicity. Other risk factors for ami- noglycoside-induced AKI are diabetes mellitus, concomitant use of other nephrotoxic drugs, prolonged use, excessive blood levels, or repeated exposure to separate courses of aminoglycoside therapy over a short time interval. We suggest that, in patients with normal kidney function in steady state, aminoglycosides are administered as a single dose daily rather than multiple-dose daily treatment regimens. Aminoglycoside demonstrates concentration-dependent bac- tericidal activity, with a prolonged ‘‘postantibiotic effect’’, thereby permitting extended interval dosing in an effort to optimize efficacy and minimize toxicity. Single-dose daily or extended-interval dosing of aminoglycosides offer a number of theoretical and practical advantages to maintain antimicrobial activity while limiting possible nephrotoxicity. This convenient and inexpensive aminoglycoside dosing strategy has been widely adopted at many centers when using this potentially toxic, yet highly effective, class of antibiotics. When feasible in patients with normal and stable kidney function, once-daily (often referred to as extended-interval) dosing of aminoglycosides should be used to limit amino- glycoside nephrotoxicity. The pharmacokinetic and pharma- codynamic properties of aminoglycosidesfavor high dosing strategies with extended intervals between doses. Aminoglycosides induce a prolonged postanti- biotic effect (inhibition of bacterial growth after blood levels have fallen below the MIC of the organism). The length of the postantibiotic effect is directly related to the peak blood levels. These pharmacokinetic/pharmacodynamic parameters make single-dose daily strategies an attractive option when using aminoglycosides. of aminoglycosides through a receptor known as megalin, expressed on epithelial cells along the proximal convoluted tubule.Aminoglycosides are concentrated in the proximal convoluted tubules, where they bind avidly to polyanionic, phospholipid-containing membranes.As the receptor uptake of aminoglycosides is saturable, high- level intermittent doses of aminoglycosides actually reduced the daily uptake and accumulation of aminoglycosides when compared to multiple-daily dosing strategies. . The cumulative results of this evidence-based review and numerous meta-analyses indicate that once-daily dosing strategies generally tend to result in less AKI when compared to multiple-dose dosing strategies, although the benefit accrued by the single-daily dose strategy is modest and inconsistent across a number of these studies. It should be noted that multiple-daily dosing strategies continue to be the standard of care for enterococcalendocarditis; no detailed, randomized trials have been reported comparing single-daily vs. multiple-daily regimens for enterococcalendocarditis. The high-dose, once-daily amino- glycoside regimens should be administered over 60minutes to avoid untoward events such as neuromuscular blockade. This recommendation is particularly important when patients are receiving other potential neuromuscular block- ing agents, or have underlying disorders affecting neuro- muscular transmission (e.g., myasthenia gravis). We recommend monitoring aminoglycoside drug levels when treatment with multiple daily dosing is used for more than 24 hours. For these reasons, therapeutic drug monitoring, in combination with or independent from, single-dose daily treatment regimens is recommended.318–321 When using therapeutic drug monitor- ing in single-dose or extended-dose treatment strategies, the Cmax should be at least 10-fold greater than the MIC of the infecting microorganism. This Cmin (trough level) should be undetectable by 18–24 hours to limit accumulation of aminoglycosides in renal tubular cells and to minimize the risk of AKI. The usual dosing strategy for once-daily aminoglycosides is 5mg/kg/d for gentamicin and tobramycin (with normal renal function); 6mg/kg/d for netilmicin; and 15mg/kg/d for amikacin. The changing pharmacokinetics and pharma- codynamics of antibiotics in general and aminoglycosides in particular, in the critically ill patient, are such that the avoidance of single-daily dosing and application of frequent therapeutic drug monitoring is indicated.3223.8.5: We suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible and suitable. Aminoglycoside aerosol delivery systems are now in use to provide high intrapulmonary antibiotic levels with minimal systemic and kidney concentrations of the antibiotic. This strategy has been used successfully in cystic fibrosis patients for the management of difficult-to-treat Gram-negative bacillary pneumonia.
  • Many nephrologists initiate dialysis for AKI empirically when the BUN exceeds 100 mg/dL in patients without clinical signs of recovery of kidney function. Initiate RRT emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist. (Not Graded) 5.1.2: Consider the broader clinical context, the presence of conditions that can be modified with RRT, and trends of laboratory tests—rather than single BUN and creatinine thresholds alone—when making the decision to start RRT. (Not Graded)

Acute kidney injury Presentation Transcript

  • 1. Acute Kidney Injury Siddhesh Kalantri Medicine Unit-1 GNDH Amritsar
  • 2. Epidemiology • 5–7% of acute care hospital admissions • 30% of admissions to the intensive care unit ( mortality rates may exceed 50%.) •India- community acquired, yet 90% being potentially reversible •Developed nations AKI is almost hospital-acquired occurring in an ICU setting
  • 3. TOP FIVE CAUSES OF AKI IN INDIA 1. Diarrhoeal diseases. 2. Sepsis: Pregnancy related septicaemia. 3. Acute Malaria- P.falciparum. 4. Drug induced. 5. Hospital Acquired.
  • 4. Definition: Kidney Disease Improving Global Outcomes (KDIGO)
  • 5.  Increase in SCr by ≥0.3mg/dl ( 26.5lmol/l) within 48 hours;  Increase in SCr to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days;  Urine volume < 0.5ml/kg/h for 6 hours.
  • 6. Risk Injury Failure Loss of function End-Stage Renal disease Rifle Criteria for stratifying AKI
  • 7. Risk  Increase in Cr of 1.5-2.0 X baseline or  urine output < 0.5 mL/kg/hr for more than 6 hours. Injury Failure Loss of function End-Stage Renal disease
  • 8. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for more than 6 hrs Injury  increase in Cr 2-3 X baseline (loss of 50% of GFR) or  urine output < 0.5 mL/kg/hr for more than 12 hours. Failure Loss of function End-Stage Renal disease
  • 9. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure  increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or  an increase in serum creatinine greater than 4 mg/dL, or  urine output < 0.3 mL/kg/hr for more than 24 hours or anuria for more than 12 hours. Loss of function End-Stage Renal disease
  • 10. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours Loss of function  persistent renal failure (i.e. need for dialysis) for more than 4 weeks. End-Stage Renal disease
  • 11. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr > 24 hrs or anuria for more than 12 hours Loss of function: Need for dialysis for more than 4 weeks End-Stage Renal disease  persistent renal failure (i.e. need for dialysis) for more than 3 months.
  • 12. Classification Patho-Physiological basis :  I. Pre-renal  II. Intrinsic  III. Post-renal
  • 13. Classification of AKI (ARF) Acute Kidney Injury Pre-renal Intrinsic Post-renal Glomerular Interstitial VascularTubular 55% 40% 5% 85%10%<5% <5%
  • 14. Oliguric Vis-à-vis Non- oliguric AKI: Non- Oliguric: In hospital set-up, secondary Nephrotoxic agents. Non-oliguric has better prognosis than oliguric one.
  • 15. ICU vs. Non-ICU AKI:  Non-ICU AKI, in which the kidney is usually the only failed organ, with mortality rates of up to 10%.  ICU AKI is often associated with sepsis and with non-renal multi-organ system failure), with mortality rates of over 50%
  • 16. Diagnosis  History and Physical examination: Pre-renal:  History: vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.  Examination : Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia
  • 17. Post- Renal: Colicky flank pain radiating to the groin suggests acute ureteric obstruction.  Nocturia and urinary frequency or hesitancy can be seen in prostatic disease. Abdominal fullness and suprapubic pain can accompany massive bladder enlargement. Definitive diagnosis of obstruction requires radiologic investigations.
  • 18.  Review all medications • Cause of AKI . • Dose Adjustment.  Systemic vasculitis with Glomerulonephritis: • Palpable purpura • Pulmonary hemorrhage, • Sinusitis.  Atheroembolic • Livedo reticularis and other signs of emboli to the legs.  Rhabdomyolysis. • Signs of limb ischemia
  • 19. Blood Tests  CBC,  BUN/creatinine,  Electrolytes,  Uric acid,  PT/PTT,
  • 20. Urine Analysis  Volume  Proteinuria  Urinary Indices: FENA and Urinary Sodium  Sediments
  • 21. Radiologic studies  Renal ultrasound (useful for obstructive forms)  Doppler (to assess renal blood flow)  CT Scan  Pyelography  Nuclear Medicine Scans : DMSA: anatomy. DTPA and MAG3: renal function, urinary excretion and upper tract outflow.
  • 22. Creatinine is a functional marker of organ damage Functional Markers: Old and Busted
  • 23. Biomarkers are Foot Prints of Actual Organ Damage Biomarkers, New Hotness
  • 24. •Cystatin C •Neutrophil gelatinase-associated lipocalin(NGAL) •Interleukin-18 •Kidney injury molecule-1 •N-acetyl-D-glucosaminidase. Important Biomarkers:
  • 25. Cystatin-C  Superior to serum creatinine, as a surrogate marker of early and subtle changes of kidney function.  It identifies kidney injury while creatinine levels remain in the normal range.  Allows detection of AKI, 24-48 hours earlier than serum creatinine
  • 26. Kidney Injury Molecule-1 (KIM-1)  KIM-1 is a type 1 trans-membrane glycoprotein  Served as a marker of severity of AKI  Can be used to predict adverse outcomes in hospitalized patients better than conventionally used severity markers.
  • 27. Neutrophil gelatinase-associated lipocalin(NGAL)  NGAL is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 hours of cardiopulmonary bypass–associated AKI.  Considered equivalent to troponin in acute coronary syndrome.
  • 28. Complications  Uremia  Hypervolemia and Hypovolemia  Hyponatremia  Hyperkalemia  Hyperphosphatemia and Hypocalcemia  Bleeding  Infections  Cardiac Complications.  Malnutrition
  • 29. Treatment
  • 30. General Isssues 1. Optimization of systemic and renal hemodynamics through volume resuscitation and judicious use of vasopressors 2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs, aminoglycosides) if possible 3. Initiation of renal replacement therapy when indicated
  • 31. Pre-Renal AKI  Prevention and treatment of prerenal azotemia requires optimization of renal perfusion.  Severe acute blood loss should be treated with packed red blood cells.
  • 32. FLUIDS  KDIGO suggest using isotonic crystalloids rather than colloids (albumin or starches) .  Colloids may be chosen in some patients to avoid excessive fluid administration in patients requiring large volume resuscitation, or in specific patient subsets (e.g., a cirrhotic patient with spontaneous peritonitis, or in burns).  Colloids- Albumin is renoprotective and Hyperoncotic starch shows nephro- toxicity.
  • 33. Vasopressors  The Work Group emphasized that vasoactive agents should not be withheld from patients with vasomotor shock over concern for kidney perfusion.  Indeed, appropriate use of vasoactive agents can improve kidney perfusion in volume- resuscitated patients with vasomotor shock.  The use of dopamine was associated with a greater number of adverse events than Nor- epinephrine.
  • 34. Low Dose Dopamine • Its use has been abandoned by most subsequent to negative results of various studies . • KDIGO recommends not using low-dose dopamine to prevent or treat AKI. (1A)
  • 35. Cirrhosis and Hepatorenal Syndrome  Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis.  Bridge therapies that have shown promise include terlipressin (a vasopressin analog), combination therapy with octreotide (a somatostatin analog) and midodrine (an α 1-adrenergic agonist), and norepinephrine, all in combination with intravenous albumin (25–50 mg per day, maximum 100 g/d).
  • 36. Cardio-Renal Syndrome  Optimization of cardiac function .  May require use of inotropic agents, preload- and afterload-reducing agents,antiarrhythmic drugs, and mechanical aids such as an intraaortic balloon pump.
  • 37. Intrinsic Acute Kidney Injury
  • 38. Diuretic • Renoprotective : Potentially lessening ischemic injury. • Can also be harmful, by worsening established AKI. • No evidence of incidence reduction. • KDIGO recommend not using diuretics to prevent AKI. (1B) • KDIGO suggest not using diuretics to treat AKI, except in the management of volume overload. (2C) • Indicated only for management of fluid balance, hyperkalemia, and hypercalcemia.
  • 39. FENOLDOPAM  Fenoldopam mesylate is a pure dopamine type-1 receptor agonist  Without systemic adrenergic stimulation.  No conclusive studies available.  For critically ill patients with impaired renal function, a continuous infusion of fenoldopam 0.1mg/kg/min improves renal function when compared to low dose dopamine.
  • 40. Erythropoietin • Recent animal studies suggest a potential clinical benefit of erythropoietin in AKI. • The renoprotective action of erythropoietin may be related to pleomorphic properties including antiapoptotic and antioxidative effects, stimulation of cell proliferation, and stem- cell mobilization. • Although one recent RCT in the prevention of human AKI was negative, the usefulness of erythropoietin in human AKI should be further tested in RCTs.
  • 41. Growth factor intervention • IGF-1 is a peptide with renal vasodilatory, mitogenic and anabolic properties. • KDIGO Work Group recommends against its use in patients with AKI.
  • 42. Rhabdomyolysis • Aggressive volume repletion (may require 10 L of fluid per day). • Alkaline fluids are beneficial. • Diuretics may be used if fluid repletion is adequate and there is no urinary output. • Dialysis. • Focus on calcium and phosphate status because of precipitation in damaged tissue.
  • 43. Glomerulonephritis or Vasculitis • May respond to immunosuppressive agents and/or plasmapheresis . • Allergic interstitial nephritis due to medications requires discontinuation of the offending agent. • Glucocorticoids have been used, but not tested in randomized trials. • AKI due to scleroderma (scleroderma renal crisis) should be treated with ACE inhibitors.
  • 44. Aminoglycoside Induced AKI • KDIGO suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephro - toxic, therapeutic alternatives are available. • Avoid in high risk patients age more than 65 years, DM, cases of septic shock. • KDIGO suggests using single dose daily rather than multiple- dose daily treatment regimens. • It also suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible .
  • 45. AMPHOTERICIN B NEPHROTOXICITY • KDIGO suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. • KDIGO recommend using azole antifungal agents and/or the echinocandins rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. • Some studies indicate that the liposomal form of amphotericin B is less nephrotoxic than amphotericin B lipid complex or amphotericin B colloidal dispersion.
  • 46. Postrenal  Prompt relief of urinary tract obstruction.  Relief of obstruction is usually followed by an appropriate diuresis and may require continued administration of intravenous fluids and electrolytes for a period of time.
  • 47. Indications for Dialysis  A – Acidosis  E – Electrolyte disturb., usually hyperkalemia  I – Intoxications (lithium, ethylene glycol, etc)  O – Overload (volume overload)  U – Uremia (symptoms, signs )
  • 48. Modes Of Dialysis  Hemodynamically stable- IHD  Hemodynamically unstable 1. CRRT 2. PD 3. SLED (Slow Low-efficiency dialysis).
  • 49. Prognosis  Pre-renal and Post- renal better prognosis.  Kidneys may recover even after dialysis requiring AKI.  10% of cases requiring dialysis develop ckd.  Die early even after kidney function recovers completely.
  • 50. Carry Home Message  Diagnose early – Biomarkers have great potential.  Look for Aetiology.  Prevent rather than treat.  No role of low dose dopamine, diuretics in prevention and treatment.  Initiate RRT when indicated.
  • 51. Thank You