552 UNIT VIII RENAL AND UROLOGICAL DISORDERS
which are DNA breakdown products. These can over- whelm the nephron tubules. Postrenal AKI develops secondary to obstruction of urine outflow. Obstruction of urine outflow leads to retrograde pressure and interference with glomerular filtration in the involved kidney. There is an abrupt increase in intratubular pressure within the nephrons that can cause AKI. Obstruction can occur in nephro- lithiasis, ureteral stricture, prostatic enlargement, or obstructive bladder disorders. Approximately 5% of AKI cases are caused by postrenal etiologies. Pathophysiology Decreased glomerular filtration of the blood in AKI leads to azotemia, high serum creatinine, and fluid retention. AKI can be divided into four phases: 1. Initial The initial phase usually last hours or days and is determined as the time from the precipitating insult until the time of initial manifestations of AKI. The oli- guric phase is associated with a significant decrease in GFR, as well as retention of urea, potassium, sulfate, and creatinine. Urine formation is usually decreased during this time and is accompanied by signs of fluid overload. The nephrons are filled with WBCs, and inflammation occurs. In the diuretic phase, the kid- neys are beginning to recover from the initial insult. Healing occurs, and fibrotic tissue may begin to form in regions of damaged nephrons. The urine output is high; however, it may not be sufficiently concentrated or diluted. Urine may have the same osmolarity as the bloodstream. This indicates that the kidney is excret- ing urine that does not contain all waste products from the bloodstream. The recovery phase is the time needed for final repair of renal damage and usually starts with the onset of increased urine output. During this phase, nephrons that are healthy compensate for those nephrons that are damaged. The undamaged neph- rons demonstrate hyperfiltration and hypertrophic 2. Oliguria 3. Diuresis 4. Recovery
changes and can perform normal clearance of solutes from the bloodstream. During the recovery phase, urine is appropriately concentrated, inflammation is diminished, and renal function returns to normal. This stage can last months, and scar tissue is apparent in
regions of kidney damage. Clinical Presentation
The patient’s clinical presentation is influenced by the cause of AKI. For example, AKI caused by autoimmune disease will present with different symptoms than AKI due to renal trauma. However, regardless of etiology, AKI causes oliguria and fluid overload. Nitrogenous waste builds up in the blood, and signs and symptoms of uremia, such as encephalopathy, anemia, hyper- kalemia, metabolic acidosis, thrombocytopenia, and neuromuscular irritability, occur. Encephalopathy can be manifested as confusion, disorientation, to a stuporous mental change depending on the severity of the kidney dysfunction. Hyperkalemia can cause cardiac rhythm changes and requires continuous ECG monitoring. Thrombocytopenia can cause sponta- neous bleeding or bruising. As urine output decreases, signs of fluid overload, such as edema of the face and extremities, occur. Pulmonary edema can develop, causing respiratory distress. Arterial blood gases should be monitored. As renal function returns, the patient demonstrates a diuresis phase, with urine out- put increasing to 1 to 2 liters per day and resolution of hypervolemia. Diagnosis The presence of AKI is defined by an elevation in the serum creatinine or reduction in urine output. AKI is confirmed by a rise in serum creatinine by at least 0.3 mg/ mL within 48 hours or at least 50% higher than base- line within 1 week, or a reduction in urine output greater than 0.5 mL/kg/hr longer than 6 hours. The stage of AKI is determined using these parameters (see Table 22.2). Anuria usually does not occur in AKI; whereas oliguria (less than 400 mL/24 hours) is common. Urinalysis, serum electrolytes, serum creatinine, BUN, arterial blood gases, protein biomarkers, and CBC
TABLE 22-2. Stages of AKI KIDNEY DISEASE: IMPROVING GLOBAL OUTCOMES STAGING OF AKI IN ADULTS
Stage
Serum Creatinine
Urine Output
1.5–1.9 times baseline (or ≥ 0.3 mg increase)
< 0.5 mg/kg/h for 6–12 hrs < 0.5 mg/kg/h for ≥ 12 hrs
Stage 1
Stage 2
2.0–2.9 times baseline
> 3 times baseline or > 4 mg/dL or initiation of renal replacement treatment
< 0.3 mg/kg/h for ≥ 24 hrs or anuria ≥ 12 hrs
Stage 3
From: Acute Kidney Injury Work Group (2012). Kidney disease: Improving global outcome (KDIGO). KDIGO clinical practice guidelines for acute kidney injury. Kidney Int Suppl, 2 (suppl 1), 19.
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