granulomatosis with polyangiitis may have AIN with or without diseaseassociated glomerular disease Patients with Sjögren syndrome and sarcoidosis also have increased risk Presenting symptoms are often nonspecific and may indicate generalized AKI, such as nausea and malaise Approximately 50% of patients will have oliguria Systemic symptoms such as rash or fever may be present A small portion of patients may complain of gross hematuria Clinical assessment The clinical assessment should focus on identifying potential symptoms of kidney dysfunction and possible underlying causes for AIN A detailed medication history including current and recently discontinued drugs should be obtained The physical examination should look for signs of systemic infections or diseases that could act as the causative factor Nephrotic syndrome is rare in the setting of AIN Proteinuria and edema are unlikely to be present Depending on the degree of underlying AKI, blood pressure may be normal Microscopic examination of the urine may reveal the presence of red blood cells or white blood cell casts Eosinophiluria defined by >1% eosinophils on the urine white blood cell differential may be suggestive of AIN but is not specific Furthermore, absence of this finding has poor negative predictive value Serum creatinine levels are almost universally elevated, and serum electrolytes should be measured Eosinophilia is evident on a CBC in approximately one-third of cases Management If an offending medication is identified as the likely cause, it should be discontinued immediately if not already done so Underlying infections should be treated Patients may require management of fluid, electrolyte, and acid–base disturbances, depending on the level of underlying renal dysfunction Rhabdomyolysis Goals of Treatment The goals of treatment for rhabdomyolysis include identifying and treating the underlying cause of the rhabdomyolysis, if possible The prevention of AKI should be achieved via aggressive hydration and measures aimed at the mitigation of renal and electrolyte abnormalities that occur must be taken Pain control may be required CLINICAL PEARLS AND PITFALLS Myoglobinuria will cause a false positive for blood on urine dipstick testing, but microscopic analysis will not be consistent with hematuria Hyperkalemia may result from both lysis of muscle cells as well as AKI Hydration is the mainstay of management Clinical Considerations Clinical recognition Rhabdomyolysis is the necrosis of muscle cells leading to introduction of intracellular contents, including myoglobin, into the blood stream The classic symptoms of rhabdomyolysis include myalgias, weakness, and red or brown urine, though this triad is not always present Rhabdomyolysis may be from traumatic or nontraumatic causes Traumatic etiologies include crush injuries, vascular occlusions, and lower extremity compartment syndrome Nontraumatic causes include extreme exertion, prolonged seizure, malignant hyperthermia, DKA, hypokalemia, hypophosphatemia, metabolic myopathies, neuroleptic malignant syndrome, and cardiac arrest It has also been associated with a variety of infections, including influenza A and B, parainfluenza, coxsackievirus, EBV, herpes simplex virus, varicella zoster, human immunodeficiency virus, pyomyositis, necrotizing fasciitis, and sepsis Prescription medications, such as statins, antipsychotics, and colchicine, and illicit drugs such as cocaine, ecstasy, and amphetamines, may cause rhabdomyolysis as well AKI during rhabdomyolysis is often multifactorial, and insults include prerenal physiology, tubular cell damage, and tubular obstruction Decreased intravascular volume and prerenal physiology develop secondary to fluid sequestration within damaged muscle and intrarenal vasoconstriction Unlike hemoglobin, myoglobin is a monomer and is freely filtered into the urine Rhabdomyolysis leads to AKI through formation of intratubular casts Tubular cell injury results from tubular obstruction with heme pigment casts and lipid peroxidation from hydroxyl radicals generated by heme and free iron Clinical assessment Laboratory results reflect the release of myocyte contents into the blood stream and include elevated serum CK as well as potential electrolyte derangements such as hyperkalemia, hyperphosphatemia, and hypocalcemia which may occur independently from AKI but be further exacerbated if renal dysfunction is present The severity of rhabdomyolysis ranges from asymptomatic elevations in serum muscle enzymes to oliguric AKI associated with life-threatening electrolyte abnormalities AKI is generally associated with serum CK levels >5,000 units/L although identifying patients at risk for developing renal complications may be difficult using the initial measurement as the value may continue to rise if there is ongoing muscle injury Clinical factors increasing the risk for AKI at lower concentrations of serum CK include dehydration, metabolic acidosis, and sepsis In the setting of myoglobinuria a urine dipstick will test positive for heme, but microscopic evaluation will be negative for red blood cells The urine sediment may reveal pigmented granular casts and a red to brown discoloration of the urine supernatant Management The mainstay of therapy for rhabdomyolysis includes early vigorous hydration to ensure adequate intravascular volume and promote urine flow The benefit of high urine flow is the removal of obstructing pigmented casts, which initiate the cytotoxic insults Children should be given IV isotonic saline to ensure adequate renal perfusion Urine output should be monitored closely The IV fluid rate will depend on the urine flow rate and should be reevaluated regularly to avoid volume excess A minimum urine flow rate of approximately to mL/kg/hr should be targeted Should the urine flow be low despite adequate volume status, a trial of furosemide 0.5 to mg/kg IV could be considered and should be continued (i.e., every to hours) if effective If diuretics are used, careful attention should be given to volume balance and perfusion to avoid concomitant prerenal insult The clinical benefits of urine alkalinization or mannitol diuresis are not proven Should metabolic acidosis develop, this may be treated with addition of bicarbonate to IV fluids The risk of providing bicarbonate is excessive alkalinization and reduction of ionized calcium in patients with evolving hypocalcemia For those with severe AKI associated with oligoanuria and electrolyte disturbance, RRT may be required until renal recovery is achieved NEPHROTIC SYNDROME CLINICAL PEARLS AND PITFALLS Nephrotic syndrome is characterized by edema, hypertension, proteinuria, hypoalbuminemia, and hyperlipidemia The most common cause in childhood is minimal change disease (MCD) Patients may be intravascularly depleted despite signs of overall fluid overload Children with nephrotic syndrome are at increased risk for serious bacterial infections and thrombosis Current Evidence Nephrotic syndrome is the clinical expression of a variety of glomerular diseases and can be classified as primary (without evidence of systemic illness), secondary, or congenital Primary nephrotic syndrome includes idiopathic nephrotic syndrome and nephrotic syndrome associated with primary glomerulonephritis Secondary nephrotic syndrome is associated with systemic disorders such as chronic hepatitis B infection and SLE Nephrotic syndrome diagnosed within the first months of life is termed congenital nephrotic syndrome; when it is diagnosed between and 12 months of life, it is called infantile nephrotic syndrome Most of these children have a genetic basis for renal disease Congenital nephrotic syndrome may also be due to intrauterine infection, such as congenital syphilis, toxoplasmosis, CMV, human immunodeficiency virus, and other organisms In children younger than 16 years, the annual incidence of nephrotic syndrome is approximately per 100,000 Presentation within the first year of life is uncommon, and nephrotic syndrome within the first months of life should raise the suspicion for congenital nephrotic syndrome Idiopathic nephrotic syndrome is the most common form of childhood nephrosis with