on 07-Aug-2017 (Mon)

Arabists should analyze the ways in which generations of amateur audiences reinterpreted old literature in order to breathe new life into traditional texts, which can turn cold and alien. Without an analysis of audience reception, we are left with a canon detached from the particular needs and choosy sensibilities of those who exercised the privilege of selecting texts for future transmission—or not.

this risk of graft loss and overall mortality increase with the length of dialysis prior to transplant

study did not detect a significant protective effect of protein-restricted diets in preventing progression of kidney disease. However, low protein diets may delay onset of symptomatic uremia in patients with late-stage CKD (stage G4/G5).

Alcoholic ketoacidosis occurs in patients with chronic ethanol abuse and liver disease and develops following an episode of acute intoxication, at which time the ingested ethanol may have already been extensively metabolized, leading to low or normal serum ethanol levels. Ethanol is oxidized to acetaldehyde and then to acetic acid,

D-Lactic acidosis is an uncommon cause of increased anion gap metabolic acidosis that is typically identified in patients with small-bowel bacterial overgrowth.

Rhabdomyolysis is a diagnostic consideration in a patient with a history of alcohol abuse and an anion gap metabolic acidosis, but this condition is frequently associated with hyperkalemia, hyperphosphatemia, hypocalcemia, and a urinalysis positive for blood with no erythrocytes visible on urine microscopy.

IgA vasculitis is associated with abdominal pain, palpable purpura, arthralgia, and glomerulonephritis, with normal complement levels.

Infection-related glomerulonephritis such as endocarditis activates the alternative pathway of complement with low C3 and normal C4 levels. The classical pathway of complement is activated with cryoglobulinemic vasculitis (C4, and sometimes C3, is depressed) and systemic lupus erythematosus (both C3 and C4 are low).

cryoglobulinemic vasculitis is associated with hepatitis C virus infection,

Hypokalemia due to vomiting is associated with metabolic alkalosis, increased urine potassium excretion, and decreased urine chloride excretion.

Hypovolemia activates the renin-angiotensin system with an increase in sodium-hydrogen exchange and increased bicarbonate reabsorption in the proximal tubule due to increased luminal hydrogen ion, and exacerbated by decreased chloride available for reabsorption with sodium.

The urine chloride concentration is low (<20 mEq/L [20 mmol/L]), reflecting gastrointestinal losses and prolonged volume contraction that leads to avid reabsorption of chloride with sodium.

Bartter syndrome mimics the effect of a loop diuretic and is accompanied by increased urine sodium (>40 mEq/L [40 mmol/L]), urine potassium (>40 mEq/L [40 mmol/L]), and chloride excretion (>40 mEq/L [40 mmol/L]).

Hypokalemic periodic paralysis is due to a shift of potassium into cells and is not associated with a metabolic alkalosis; furthermore, urine potassium would be low (<20 mEq/L [20 mmol/L]) and not increased.

Shiga toxin–associated hemolytic uremic syndrome is a diarrhea- associated syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and kidney failure caused by Shiga toxin– producing Escherichia coli.

Ultrasonography is the preferred diagnostic imaging modality for pregnant patients with suspected nephrolithiasis because it does not expose patients to radiation.

Transvaginal ultrasonography may be used to detect distal ureteral stones in pregnant women with suspected nephrolithiasis and an unrevealing kidney ultrasound.

Patients with enteric hyperoxaluria and calcium oxalate nephrolithiasis may benefit from treatment with bile salt binders to decrease intestinal oxalate absorption.

Treatment with cholestyramine is an appropriate additional therapy for this patient with enteric hyperoxaluria.

Thiazide diuretics, such as hydrochlorothiazide, are used in patients with idiopathic hypercalciuria to reduce calcium excretion in the urine by inducing mild hypovolemia that results in increased sodium reabsorption and passive calcium reabsorption in the proximal tubule.

Urine citrate inhibits stone formation by binding calcium in the tubular lumen, preventing it from precipitating with oxalate. Citrate excretion can be enhanced in patients with low urine citrate levels by alkalinizing the serum with potassium citrate, which decreases uptake of filtered citrate from the tubular lumen.

The expected compensation for chronic respiratory alkalosis is a decrease in the serum bicarbonate of 4 to 5 mEq/L (4-5 mmol/L) for each 10 mm Hg (1.3 kPa) decrease in the PCO2. The expected serum bicarbonate concentration in this patient is calculated to be 14 to 16 mEq/L (14-16 mmol/L), and the measured serum bicarbonate of 20 mEq/L (20 mmol/L) suggests coexistence of a metabolic alkalosis.

Calculating the ratio of the change in the anion gap (Δ anion gap) to the change in bicarbonate level (Δ bicarbonate), or the “Δ-Δ ratio,” can help confirm if there is a coexisting acid-base disturbance. A ratio of <1 may reflect the presence of concurrent normal anion gap metabolic acidosis, whereas a ratio of >2 may indicate the presence of metabolic alkalosis

Evidence for a tubulointerstitial process includes a slowly progressive course without a clear inciting event, subnephrotic proteinuria, bland urine sediment, and a kidney ultrasound showing atrophic kidneys

An associated characteristic that may be present with tubulointerstitial disease is abnormal tubular handling of glucose, amino acids, uric acid, phosphate, and bicarbonate (termed Fanconi syndrome);

Hypertensive nephropathy involves damage to the vascular structures, glomeruli, and tubulointerstitial regions of the kidney. It may cause progressive kidney failure, often with elevated protein excretion (less than 1000 mg/24 h).

Membranoproliferative glomerulonephritis may also be associated with chronic hepatitis B infection and involves immune complex deposition in the glomeruli. It typically presents with hematuria (often with dysmorphic erythrocytes and/or erythrocyte casts), variable degrees of proteinuria, and a reduced glomerular filtration rate.

Membranous glomerulopathy is common in patients with chronic hepatitis B infection and appears to be related to subendothelial and mesangial immune deposits in the glomeruli. Because it primarily affects the glomeruli, it is associated with high levels of proteinuria, usually in the nephrotic range,

Intravenous dextrose-containing fluids can exacerbate hypophosphatemia by stimulating insulin release, which promotes phosphate uptake by the cells and worsening hypophosphatemia.

The most likely cause of this patient's respiratory failure is hypophosphatemia, which occurs in patients with chronic alcohol use, malnutrition, or critical illness. Symptoms rarely occur unless the serum phosphate concentration is <2.0 mg/dL (0.65 mmol/L); severe symptoms occur with a serum phosphate concentration <1.0 mg/dL (0.32 mmol/L). Symptoms include weakness, myalgia, rhabdomyolysis, arrhythmias, heart failure, respiratory failure, seizures, coma, and hemolysis.

Severe hypophosphatemia can cause respiratory failure from impaired diaphragmatic contractility

All NSAIDs contribute to hypertension by inhibition of cyclooxygenase-2 in the kidneys, promoting sodium retention and increased intravascular volume.

Additional effects of NSAIDs include hyperkalemia

Manifestations of D-lactic acidosis include intermittent confusion, slurred speech, ataxia, and an increased anion gap metabolic acidosis with a normal plasma lactate level.

This patient has an increased anion gap metabolic acidosis, and the most likely cause is D-lactic acidosis. Accumulation of the D-isomer of lactate can occur in patients with short-bowel syndrome following jejunoileal bypass or small-bowel resection

Ethylene glycol or methanol intoxication should be suspected in patients with an increased anion gap metabolic acidosis associated with a serum bicarbonate level <10 mEq/L (10 mmol/L) and a plasma osmolal gap >10 mOsm/kg H 2 O.

Pyroglutamic acidosis is a cause of increased anion gap metabolic acidosis in patients receiving therapeutic doses of acetaminophen on a chronic basis. Clinical manifestations are limited to mental status changes and increased anion gap metabolic acidosis. The syndrome most commonly occurs in patients with critical illness, poor nutrition, liver disease, or chronic kidney disease as well as in persons on a vegetarian diet. Diagnosis can be confirmed by measuring urine levels of pyroglutamic acid.