Hectoral (doxercalciferol) injection [package insert]. Cambridge, MA: Genzyme Corporation; 2012.
Hectoral (doxercalciferol) capsules [package insert]. Cambridge, MA: Genzyme Corporation; 2011.
chronic kidney disease. Clin J Am Soc Nephrol. 2009;4(9):1529–1539.
evidence review. Semin Dial. 2015;28(5):497–507.
Sensipar (cinacalcet) [package insert]. Thousand Oaks, CA: Amgen; 2014.
hyperparathyroidism. Am J Nephrol. 2007;27(3):274–278.
N EnglJ Med. 2012;367(26):2482–2494.
cinacalcet HCl in participants with CKD not receiving dialysis. Am J Kidney Dis. 2009;53(2):197–207.
J Am Soc Nephrol. 2015;10(1): 90–97.
Leavey SF, Weitzel WF. Endocrine abnormalities in chronic renal failure. Endocrinol Metab Clin N Am.
Holley JL, Schmidt RJ. Sexual dysfunction in CKD. Am J Kidney Dis. 2010;56(4):612–614.
United States cohort comparison. J Am Soc Nephrol. 2014;25(5):1103–1109.
Akalin N et al. Comparison of insulin resistance in the various stages of chronic kidney disease and
inflammation. Ren Fail. 2015;37(2):237–240.
disease patients. Clin Cardiol. 2011;34(6):360–365.
Bailey JL. Insulin resistance and muscle metabolism in chronic kidney disease. ISRN Endocrinol.
Galbusera M et al. Treatment of bleeding in dialysis patients. Semin Dial. 2009;22(3):279–286.
Mettang T, Kremer AE. Uremic pruritus. Kidney Int. 2015;87(4):685–691.
Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO clinical
practice guideline for glomerulonephritis. Kidney Int Suppl. 2012;2:139–274.
Lupus Epidemiology and Surveillance program. Arthritis Rheumatol. 2014;66(2):369–378.
controlled trial and long-term follow-up. Ann Rheum Dis. 2016;75(1):30–36.
lupus nephritis: a clinical observationalstudy. Rheumatology. 2014;53(9):1570–1577.
Schilder AM. Wegener’s Granulomatosis vasculitis and granuloma. Autoimmun Rev. 2010;9(7):483–487.
Hiemstra TF et al. Mycophenolate mofetil vs azathioprine for remission maintenance in antineutrophil
Science. 2010;329(5993):841–845.
Acute kidney injury (AKI) is characterized clinically by an abrupt
decrease in renal function over a period of hours to days, resulting in the
accumulation of nitrogenous waste products (azotemia) and the inability
to maintain and regulate fluid, electrolyte, and acid–base balance.
Risk factors for the development of AKI include older age, higher
baseline serum creatinine (SCr), chronic kidney disease (CKD),
diabetes, chronic respiratory illness, underlying cardiovascular disease,
prior heart surgery, dehydration resulting in oliguria, acute infection, and
The clinical course of AKI has three distinct phases: the oliguric phase
—a progressive decrease in urine production after kidney injury; the
diuretic phase—initial repair of the kidney insult with resultant diuresis
of accumulated uremic toxins, waste products, and fluid; and the
recovery phase—return of kidney function depending on the severity of
AKI is classified according to the physiologic event leading to AKI:
prerenal azotemia—decreased renal blood flow; functional—impairment
of glomerular ultrafiltrate production or intraglomerular hydrostatic
pressure; intrinsic—damage to the kidneys; and postrenal—outflow
obstruction in the urinary tract.
The urinalysis is an important diagnostic tool for differentiating AKI into
prerenal azotemia, intrinsic, or obstructive AKI. Urinary chemistries are
used to differentiate between prerenal azotemia and intrinsic AKI.
Medications that affect renal function (e.g., angiotensin-converting
enzyme [ACE] inhibitors, angiotensin II receptor blockers [ARBs], and
aminoglycoside antibiotics) should be dosed according to renal function
and monitored closely in patients with AKI. Nephrotoxic medications
Patients with nonoliguric renal failure have significantly better outcomes
than those with oliguria; however, converting a patient from oliguria to
nonoliguria through pharmacologic intervention does not improve patient
Hydration therapy is useful in the following ways: to increase renal
perfusion and avert the conversion of prerenal azotemia to acute tubular
necrosis (ATN), to reduce the risk of contrast-induced nephropathy
(CIN) in high-risk patients, and to prevent and treat kidney stones.
Few treatment options are available in established AKI, therefore
prevention is key. Supportive therapy is aimed at preventing the
morbidity and mortality of AKI: close patient monitoring; strict fluid,
electrolyte, and nutritional management; treatment of life-threatening
conditions, such as pulmonary edema, hyperkalemia, and metabolic
acidosis; avoidance of nephrotoxic drugs; and initiation of renal
Although diuretics have not been shown to improve patient outcomes,
they can be used to prevent complications from fluid overload. Sodium
restriction, daily monitoring of volume status, laboratory chemistries,
urine output, and gastrointestinal (GI) and insensible losses should be
measured during diuretic therapy.
RRT is reserved for patients with severe acid–base disorders, fluid
overload, hyperkalemia, or symptomatic uremia as a result of AKI.
Dosage adjustments are necessary for drugs that are removed during
Acute kidney injury (AKI) is characterized clinically by an abrupt decrease in renal
function over a period of hours to days, resulting in the accumulation of nitrogenous
waste products, urea and creatinine (azotemia), and the inability to maintain and
regulate fluid, electrolyte, and acid–base balance.
1 AKI is a devastating syndrome
with multiple risk factors or causes. It is associated with multi-organ dysfunction,
increased resource utilization, high cost, and increased mortality. Like chronic kidney
disease (CKD), AKI is common, treatable, and is also largely preventable. Not only
is underlying CKD a risk factor for AKI, but AKI also contributes to CKD
development and may result in dialysis dependency. Minimizing causes of AKI and
increasing awareness of the importance of early detection and treatment are
associated with improved outcome in AKI. Clinicians recognize a rapid approach to
treatment is essential because the causes and complications of AKI do not allow
much time to initiate management and reversal.
Many attempts have been made to objectively quantify AKI based on laboratory
data, daily urine output, or the need for renal replacement therapy (RRT) (i.e.,
dialysis). Over the past decade the working definition of AKI has evolved. Currently,
expert opinion and consensus recommend assessing quantitative serum creatinine
(SCr) changes from baseline or urinary volume. They are considered important
clinical pointers in the detection, diagnosis, and severity of AKI. Vigilant daily
assessment of these markers continues while the patient is hospitalized. In 2004, the
Acute Dialysis Quality Initiative created an international expert panel, which
proposed a new classification system called RIFLE.
stages of AKI, including risk, injury, failure, loss (defined as the need for dialysis at
least 1 month after failure), and finally end-stage renal disease (ESRD). In 2007, the
recognition that even smaller changes in SCr than defined in RIFLE might be
associated with adverse outcomes and mortality led to newer definitions by the Acute
8 The three AKIN stages map to, but are not identical
to, the RIFLE classification. The RIFLE and AKIN are very useful for quantitating
renal function for research purposes rather than clinical activities. In 2012, the
Kidney Disease Improving Global Outcomes (KDIGO)
uniform practical clinical definition of AKI, essentially merging the RIFLE and
AKIN criteria. AKI is defined as an increase in SCr > 0.3 mg/dL within 48 hours,
OR an increase in SCr > 1.5 times baseline in 7 days or less OR a decrease in urine
volume <0.5 mL/kg/hour for >6 hours. The most recent guideline provides a useful
tool to assist clinicians for managing AKI (Table 29-1).
These new classification systems provide advantages over traditional definitions,
and represent a significant step forward in detecting and preventing AKI. Future
studies need to prospectively evaluate their application in diverse clinical settings on
the basis of evidence rather than opinion or consensus and also their performance as
prognostic predictors of patient outcome. Regardless of the definitions used, the
clinician should suspect AKI when the kidney is unable to regulate fluid, electrolyte,
acid–base, or nitrogen balance, even in the presence of a normal SCr concentration.
Healthcare technology information systems are working on alerts to notify clinicians
Comments
Post a Comment
اكتب تعليق حول الموضوع