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- 1. increase of serum creatinine >50%
- 2. <0.5 cc/kg/h over 6 hrs
- 3. absolute increase of serum creatinine of 26.5 umol/L over 2 days
- 1. GFR <60 mL/min/1.73 m2
- 2. kidney damage (abn urinalysis, kidney imaging, or biopsy) of at least 3 months
- -ranges from 10:1 to 15:1 -> 20:1 (creatinine) bc it is reabsorbed more with dehydration
- -increased w: dehydration, high protein, gi bleeding, catabolic state
- -decreased w: liver failure, malnutrition
This patient has acute kidney injury (AKI), as evidenced by the sudden onset of oliguria and an increase in her blood urea nitrogen (BUN) and serum creatinine values. Her urine (normal upon admission) is positive for leukocytes and leukocyte casts, but the culture is negative (sterile pyuria). This clinical picture is most consistent with tubulointerstitial inflammation caused by acute interstitial nephritis. Drugs, particularly β-lactam antibiotics, are the most common etiology of acute interstitial nephritis. Patients may also have fever, rash, and eosinophilia, although only a minority of patients will have all three features.
- Acute tubular necrosis (ATN) is the most common form of intrarenal disease that causes acute kidney injury in hospitalized patients. Onset of this condition usually occurs after a sustained period of ischemia or exposure to nephrotoxic agents. Urinalysis in approximately 75% of patients with acute tubular necrosis reveals muddy brown casts; leukocytes and leukocyte casts are not associated with ATN.
- elevated serum creatinine level, minimal proteinuria, and muddy brown casts on urinalysis are most consistent with acute tubular necrosis. This condition usually develops after a sustained period of ischemia or exposure to nephrotoxic agents such as cisplatin, intravenous aminoglycosides, or radiocontrast.
Cholesterol crystal embolization may cause AKI
This condition may occur spontaneously but most often develops after coronary or kidney angiography or aortic surgery. Kidney injury in patients with cholesterol crystal embolization usually has a subacute onset with a stuttering course over several weeks. Cutaneous manifestations develop in approximately 10% to 15% of patients and may include livedo reticularis, skin ulceration, and nodules. Patients with cholesterol crystal embolization typically have a bland urine sediment but may have dysmorphic hematuria and erythrocyte casts.
- orthostatic hypotension, tachycardia, and the BUN-creatinine ratio >20:1
- Acute kidney injury in patients with malignancy is often due to prerenal disease, obstruction, or use of nephrotoxic agents. The presence of hypotension, hyponatremia, and a decreased urine sodium excretion accompanied by a bland urine sediment raises suspicion for prerenal azotemia.
Persistent hematuria requires cystoscopy
- presence of three or more erythrocytes/hpf in the urine detected on two or more samples. Bleeding in patients with persistent hematuria may originate anywhere along the genitourinary tract, and differentiating between glomerular and nonglomerular hematuria helps to guide management. This patient's normal-appearing erythrocytes revealed on urine microscopy and absence of erythrocyte casts and protein in the urine are consistent with nonglomerular hematuria.
- One possible cause of persistent nonglomerular hematuria is genitourinary tract malignancy. Risk factors for these malignancies include male sex, age greater than 50 years, tobacco use, and exposure to drugs such as cyclophosphamide and benzene and radiation. Because this patient has several risk factors, cystoscopy is indicated to exclude a malignancy.Hematuria may develop in patients taking NSAIDs or anticoagulants but should not automatically be attributed to these agents; appropriate evaluation for glomerular or nonglomerular disorders should still be performed in this setting. In addition, discontinuation of warfarin may place him at risk for further thromboembolic disorders.
The syndrome was first identified in patients with traumatic crush injuries, but there are nontraumatic causes, such as alcohol (due to hypophosphatemia), drug use, metabolic disorders, and infections. The classic triad of findings includes muscle pain, weakness, and dark urine. The diagnosis is based on clinical findings and a history of predisposing factors (such as prolonged immobilization or drug toxicity) and confirmed by the presence of myoglobinuria, an increased serum creatine kinase level, and, in some cases, hyperkalemia. A positive urine dipstick for blood in the absence of erythrocytes also suggests rhabdomyolysis. The disorder usually resolves within days to weeks. Treatment consists of aggressive fluid resuscitation; fluids should be adjusted to maintain the hourly urine output at least 300 mL until the urine is negative for myoglobin. Acute kidney injury resulting from acute tubular necrosis occurs in approximately one third of patients. Dialysis is sometimes necessary.
Patients with acute kidney injury (AKI) caused by urinary tract obstruction have a favorable prognosis when obstruction is relieved within 1 week of onset. A kidney ultrasound would reveal a distended bladder and possible hydronephrosis. Insertion of a Foley catheter is initial treatment.
HUS causing AKI
HUS commonly manifests as acute kidney injury (AKI) accompanied by thrombocytopenia and microangiopathic hemolytic anemia (schistocytes on peripheral blood smear). The two most common causes are infection by Shiga toxin–producing Escherichia coli(E. coli O157:H7 and other serotypes) and familial deficiency of factor H. The toxin causes bloody diarrhea and enters the circulation and binds to platelets, glomerular capillary endothelial cells, mesangial cells, and glomerular and tubular epithelial cells. Shiga toxin binds to platelets by means of globotriaosylceramide receptors, which leads to platelet aggregation. Shiga toxin may also stimulate endothelial cells to release large von Willebrand factor multimers, which can further enhance platelet aggregation. Factor H, a protein in the complement pathway, normally protects cells from damage by the alternative complement pathway. A deficiency of factor H allows C3 to potentiate autoantibody-mediated or immune complex–mediated injury to glomerular cells, leading to exposure of subendothelium and activation of both platelets and coagulation.
HTN w/ CKD
blood pressure targets of less than 130/80 mm Hg or less than 125/75 mm Hg when significant proteinuria is present. Angiotensin-converting enzyme inhibitors, such as lisinopril, and angiotensin receptor blockers (ARBs), such as losartan, are the preferred agents in chronic kidney disease and slow progression of kidney disease in patients with diabetes. These agents reduce efferent arteriolar resistance and lower intraglomerular pressure and, therefore, may be associated with increases in serum creatinine in patients with a reduced glomerular filtration rate. An increase in creatinine of up to 30% is acceptable. In this patient, blood pressure remains elevated and he has significant proteinuria. The most logical next step would be to increase losartan. It is not necessary to discontinue losartan, because the increase in creatinine is not unexpected and his potassium remains at an acceptable level.
Patients with stage 5 chronic kidney disease (glomerular filtration rate [GRF] <15 mL/min/1.73 m2 or receiving dialysis) often develop signs of uremia and require kidney replacement therapy. Absolute indications include uncontrollable hyperkalemia, uncontrollable hypervolemia, altered mental status or excess somnolence, pericarditis, or bleeding-diathesis secondary to uremic platelet dysfunction. Relative indications include nausea, vomiting, and poor nutrition caused by decreased appetite; severe metabolic acidosis; mild changes in mental status such as lethargy and malaise; asterixis; and worsening of kidney function with GFR less than 15 mL/min/1.73 m2. However, the timing of hemodialysis in patients without fluid overload, hyperkalemia, metabolic acidosis, or uremic symptoms, such as this patient, is unclear. A recent study suggests early initiation of hemodialysis does not improve patient outcomes. Kidney transplantation is the treatment of choice for uremia. Transplantation in patients who have not yet been treated with hemodialysis is associated with better patient and allograft outcomes. This patient has several family members who are willing kidney donors, and it is possible that he could receive a transplant in the near future; therefore, the best course of action would be to follow the patient closely to ensure he does not develop uremic signs or symptoms or other indications for dialysis and strive for transplantation rather than dialysis.