CHAPTER 22 Renal Disorders 551
antibodies can be used to monitor the severity of dis- ease and efficacy of treatment. Antineutrophilic cyto- plasmic antibodies (ANCAs) can also develop, and a titer for this antibody is commonly done. Urinalysis demonstrates proteinuria, hematuria, and RBC casts. The complete blood count (CBC) may show anemia secondary to pulmonary bleeding. There is leukocyto- sis, elevated BUN, and serum creatinine. Kidney biopsy may be necessary, but is preferably avoided because the kidney is a highly vascular organ and severe bleed- ing is common. Renal biopsy show focal or segmen- tal necrosis and crescent formations in the Bowman’s capsule region. Immunofluorescent staining shows IgG antibodies and complement proteins. Chest x-ray shows bilateral hilar lymphadenopathy and consolida- tions throughout both lung fields. Pulmonary function testing will reveal a restrictive disease pattern. Treatment Plasmapheresis is a process of filtering the blood that can remove anti-GBM and other antibodies. Oral predni- sone and cyclophosphamide are used with plasmapher- esis. Maintenance treatment with immunosuppressants such as rituximab or azathioprine can be used to stop further production of antibodies. Various pulmonary treatments may be needed, depending on the disorder. Dialysis or kidney transplantation may be indicated if disease deteriorates to ESRD. However, anti-GBM dis- ease can occur in the newly transplanted kidney as well. Acute Kidney Injury AKI, previously called acute renal failure, is related to an abrupt insult to the kidney that causes a rapid decrease in renal filtration function. It usually occurs in the setting of acute or chronic illness. It is a sudden decrease in glomerular filtration rate manifested by an increase in serum creatinine and oliguria. Because of this decline in function, nitrogenous waste products accumulate in the body. AKI is staged based on the magnitude of rise in serum creatinine and duration of oliguria. With appropriate interventions, normal renal function can return, usually within 2 weeks to 3 months of the initial precipitating event. Epidemiology AKI occurs in 20% of hospitalized patients yearly in the United States. In critical care units, up to 67% of patients have AKI. AKI also develops postoperatively in approximately 1% of general surgery cases. Because of an aging population and increasing prevalence of HTN and DM, from 2005 to 2014, the number of hospitalizations with a principal diagnosis of acute kidney injury increased from 281,500 to 504,600, and the number of hospitalizations with a secondary diag- nosis of acute kidney injury increased from 1 million to 2.3 million. Morbidity of AKI in those admitted to the ICU exceeds 50%. AKI increases risk for development of CKD and development of dialysis-requiring ESRD.
Etiology There are various causes of AKI, but the major cause is reduced renal blood flow that in turn reduces GFR. Acute illness, complications of medications, and med- ical procedures are the most common causes of AKI. Older age and preexisting CKD are the main suscepti- bility factors. As renal function decreases, there is an accumulation of nitrogenous wastes and impairment of fluid and electrolyte balance. AKI is frequently superimposed on other conditions affecting the patient. There are three classifications of AKI: 1. Prerenal azotemia Approximately 60% of patients suffer AKI because of prerenal azotemia disorders. The prefix “azo” means nitrogen, the suffix “emia” means in the blood. It is the designation for a rise in serum creatinine and BUN concentration due to inadequate renal blood flow to support the hydrostatic pressure needed for glomeru- lar filtration. Decreased blood flow is the major cause of prerenal AKI and is usually reversible with timely treatment. This type of AKI can occur any time there is an extreme drop in blood volume. Various shock states, including hypovolemic, cardiogenic, and septic shock, which result in decreased renal perfusion, lead to pre- renal AKI. Ischemia associated with prolonged blood loss due to hemorrhage from trauma or surgery can also cause AKI. Severe burns over the body can also cause extensive fluid loss, which causes lack of blood flow to the kidney. Prolonged renal hypoperfusion will cause damage of the nephron tubule epithelial cells, a condition known as acute tubular necrosis (ATN) . Intrinsic renal disease as a cause of AKI is due to actual damage to kidney tissue often associated with nephrotoxic agents, infectious processes, trauma, or obstruction of nephron tubules. A common cause of AKI is ATN caused by nephrotoxic agents. Common nephrotoxic agents include NSAIDs, aminoglycoside antibiotics, chemotherapeutic agents, and radiopaque dye used in imaging studies. Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) can also cause changes in the vaso- regulatory mechanisms of the kidney and can decrease perfusion leading to AKI. Infectious processes such as glomerulonephritis or pyelonephritis can cause intrin- sic AKI. Obstruction of nephron tubules can occur in disorders that cause excretion of a large amount of breakdown products from hemoglobin, myoglobin, or purines. These breakdown products in need of excre- tion can overwhelm the nephron tubules. For example, hemoglobinuria is seen in transfusion reactions and other hemolytic disorders. Myoglobinuria can occur in severe muscle trauma or extreme exertion. Excessive purines within the bloodstream occur when there is a massive tumor or cellular destruction. For example, in chemotherapy, a large amount of cellular deterio- ration occurs; tumor cell breakdown releases purines, 2. Intrinsic renal disease 3. Postrenal obstruction
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