on 14-Jul-2017 (Fri)

α-blocker doxazosin may be considered for its dual blood pressure–lowering effect and its effect on urinary frequency, its use as first-line therapy for persistent hypertension following lifestyle modification should be decided while considering its adverse effect profile (such as orthostatic hypotension) and its increased incidence of heart failure

thiazide diuretics such as hydrochlorothiazide, which increases serum urate

The finding of a nephritic urine sediment (erythrocytes, erythrocyte casts, and proteinuria) in an azotemic patient with an active infection suggests IRGN. IRGN is an immune complex–mediated disease most frequently associated with nonstreptococcal infections, with the antigen in the immune complex derived from the infectious agent. Immune complexes deposit in the subepithelial area and activate complement with recruitment of inflammatory cells, leading to a proliferative GN

Drug-induced tubular toxicity (for example, with vancomycin) typically occurs after 7 to 10 days of antibiotic therapy and the urine sediment does not show cells, unlike in this patient. Antibiotic-induced AIN is typically associated with mild proteinuria, erythrocytes, leukocytes, and leukocyte casts on urinalysis. Eosinophiluria, recurrence of fevers, rash, and peripheral eosinophilia may also be seen

isolated hematuria with a family history of hematuria may require serial measurements of kidney function and urine protein because kidney failure may occur later in life.

familial hematuric syndrome, which is typically associated with either X-linked or somatic mutations of type IV collagen. In female carriers of X-linked hereditary nephritis (Alport syndrome), kidney failure may occur later in life. Thus, annual measurements of blood pressure, kidney function, and urine protein are reasonable

Blood pressure averages ≥135/85 mm Hg by ambulatory blood pressure monitoring or home monitoring meet most consensus panels' definition of hypertension and should be treated with pharmacologic therapy

nighttime hypertension is defined by average values >125/75 mm Hg

the typical blood pressure drop from daytime to nighttime (during sleep) of approximately 15%, noted in both normotensive and hypertensive patients. A lack of blood pressure drop of at least 10% (“non-dipping”) is independently associated with left ventricular hypertrophy, cardiovascular events, moderately increased albuminuria (formerly known as microalbuminuria), and a more rapid rate of decline in glomerular filtration rate

Management of uric acid nephrolithiasis includes adequate urine output, urine alkalinization, and xanthine oxidase inhibitors if needed to decrease uric acid production.

low urine pH, markedly increase the risk of uric acid stones by favoring the development of insoluble uric acid from the relatively soluble urate salt.

Oral hydration to maintain a urine output of at least 2 L/d is the mainstay of therapy. If this is inadequate, the next treatment is urine alkalinization (usually with potassium citrate or potassium bicarbonate) to increase the solubility of uric acid.

Cholestyramine binds bile salts and oxalate in the gut and is sometimes used as a treatment for kidney stones related to hyperoxaluria but would likely not benefit this patient with uric acid stones.

Thiazide diuretics, such as hydrochlorothiazide, decrease hypercalciuria by increasing proximal sodium reabsorption and passive calcium reabsorption in the kidney. However, this is a strategy for treating calcium-based nephrolithiasis and is not effective for uric acid stones.

chronic kidney disease stage 4 and greater (glomerular filtration rate <30 mL/min/1.73 m 2 ), thiazide diuretics lose potency, and loop diuretics may often be required.

The centrally acting agent clonidine and the vasodilator minoxidil are potent antihypertensives sometimes used in cases of resistant hypertension if maximal doses of more conventional agents are unsuccessful. However, this patient is not currently on optimal triple therapy, and both agents also increase the risk of orthostatic hypotension in those with autonomic neuropathy, such as this patient. Moreover, the use of minoxidil without adequate diuresis will worsen salt and water retention and should be avoided.

Combination therapy with the ACE inhibitor lisinopril and the calcium channel blocker (CCB) amlodipine is appropriate for this patient with stage 2 hypertension, which is defined as a systolic blood pressure ≥160 mm Hg and/or a diastolic blood pressure ≥100 mm Hg

Diagnose white coat hypertension using ambulatory blood pressure monitoring

White coat hypertension is defined as blood pressure readings in the office ≥140/90 mm Hg and out-of-office readings that average <135/85 mm Hg.

Urine testing for fractionated metanephrines is used to evaluate for pheochromocytoma as a secondary cause of hypertension.

Pheochromocytoma is generally suspected in patients with the symptom triad of episodic headache, sweating, and tachycardia associated with coincident increases in blood pressure

Aminoglycoside-induced acute kidney injury typically presents as nonoliguric acute tubular necrosis with granular casts in the urine sediment and a fractional excretion of sodium >1%, and the serum creatinine characteristically rises 5 to 10 days after starting therapy

Hypokalemia and hypomagnesemia can also occur with aminoglycoside toxicity due to kidney potassium and magnesium wasting.

Cephalosporins, such as cefazolin, can cause AKI from acute interstitial nephritis. Urine findings include leukocytes, erythrocytes, and leukocyte casts. Fever, maculopapular rash, peripheral eosinophilia, and eosinophiluria can also occur. Onset of AKI after drug exposure ranges from 3 to 5 days with a second exposure, to as long as several weeks to months with a first exposure.

Cholesterol embolism occurs in patients with atherosclerotic disease after undergoing an invasive vascular procedure or receiving an anticoagulant or thrombolytic agent within the past several months. Emboli from ruptured atheromatous plaques occlude small and medium arterioles, causing ischemia and inflammation with organ dysfunction. Clinical features include rash (livedo reticularis), AKI, purple discoloration of the toes, bowel ischemia, neurologic manifestations, and eosinophilia.

Iodinated contrast can induce vasospasm and cause ischemic injury or direct damage to the kidneys. Low osmolar contrast is thought to be safer than high osmolar contrast

Contrast-induced nephropathy (CIN) is defined as either an increase in serum creatinine of 0.5 mg/dL (44.2 µmol/L) or an increase in serum creatinine of 25% from baseline at 48 hours after contrast administration.

Kidney transplant recipients are predisposed to new-onset diabetes after transplantation (often referred to as NODAT). Medications that promote development of NODAT include glucocorticoids, tacrolimus, and the mammalian target of rapamycin (mTOR) inhibitors sirolimus and everolimus.

Dyslipidemia is also a common complication posttransplantation, and commonly used immunosuppressive medications that promote dyslipidemia include cyclosporine and mTOR inhibitors.

cardiovascular disease is the leading cause of death among kidney transplant recipients

Many patients have residual hyperparathyroidism after transplant that can be slow to resolve; hypercalcemia is relatively commonly observed posttransplant but hypocalcemia is uncommon.

Mechanical stone removal is appropriate for patients with large (>10 mm) kidney stones or those with smaller stones who have failed medical management or have complicated nephrolithiasis (urosepsis, acute kidney injury, anuria, refractory pain).

Uncomplicated kidney stones <10 mm in size may usually be treated with conservative management (including hydration, analgesia, observation, and periodic re-evaluation) and medical expulsive therapy, which usually consists of either an α-blocker (such as tamsulosin) or calcium channel blocker (such as nifedipine).

The most likely diagnosis is IgG4-related interstitial nephritis. This patient has a history of autoimmune pancreatitis and now presents with acute kidney injury. Her urinalysis is most consistent with a tubulointerstitial pattern, with mild proteinuria and the presence of inflammatory cells.

Systemic IgG4-related disease is an uncommon disorder characterized by infiltration of different organs by lymphoplasmacytic infiltrates of IgG4-positive plasma cells with resultant fibrosis associated with elevated serum IgG4 levels

The first step when assessing a patient with metabolic alkalosis is to clinically assess the patient's volume status.

This patient has metabolic alkalosis as implied by the elevated serum bicarbonate and is hypovolemic as evidenced by the orthostatic blood pressure and pulse changes. Such a patient would be expected to have low urine concentrations of sodium and chloride. However, these patient’s urine electrolytes show increased excretion of sodium and chloride despite the evident hypovolemia. These findings suggest the presence of active diuretic use or a renal tubular defect that impairs handling of sodium and chloride, such as Bartter and Gitelman syndromes.

Measurement of 24-hour urine free cortisol excretion is a standard test for diagnosing Cushing syndrome, which is characterized by proximal muscle weakness, hypokalemia, hypertension, and diabetes mellitus.

Plasma aldosterone-plasma renin ratio is unlikely to be helpful in this situation. Although primary hyperaldosteronism is characterized by hypokalemia and metabolic alkalosis, the absence of hypertension makes this diagnosis unlikely

In place of the current model - two or three years of vocabulary, grammar, and conversation, fol lowed by literature courses - the new approach incorporates more culture from the start. Newspa per clippings, fiction, video clips, and advertise ments form an integral part of lessons. Students, for example, become familiar with the German used in political speeches and learn how it differs from that used in a business letter or soap opera

It appears that professional and amateur littérateurs—who were seemingly honest and intelligent—fabricated narratives in mujālasāt that they recounted as being truthful and historical. Drawing on previous scholarship on Arabic, European, and Persian historiography and literature, I argue that littérateurs employed a set of principles for speaking in assembly that need not be reconciled with our own modern principles.

Part two of the book analyzes the impact of mujālasāt on the formation of tradition