on 16-Jul-2017 (Sun)

decreased muscle mass would be expected to cause long-term decreases in the serum creatinine

serum creatinine is expected to increase by 25% to 30% with appropriate dosing of an ACE inhibitor

patient with stage G4/A3 CKD should receive the 13-valent pneumococcal conjugate vaccine (PCV-13) 1 or more years after the 23-valent pneumococcal polysaccharide vaccine (PPSV-23). A second dose of PPSV-23 should be administered 5 or more years after the first dose.

Other immunocompromising conditions that are indications for pneumococcal vaccination are anatomic and functional asplenia, congenital or acquired immunodeficiency (including B- or T-lymphocyte deficiency, complement deficiencies, and phagocytic disorders excluding chronic granulomatous disease), HIV infection, the nephrotic syndrome, leukemia, lymphoma, Hodgkin lymphoma, generalized malignancy, multiple myeloma, solid-organ transplant, and iatrogenic immunosuppression (including long-term systemic glucocorticoids and radiation therapy)

patients younger than 65 years of age with CKD who have not been previously immunized against invasive pneumococcal disease, the ACIP recommends that PCV-13 be administered first followed by PPSV-23 no sooner than 8 weeks later.

Differentiating the cause of a normal anion gap metabolic acidosis may be accomplished by measurement of the urine anion gap, which is calculated as follows: (UNa + UK − UCl). The urine anion gap is a surrogate method of estimating the ability of the kidney to excrete an acid load.

because ammonium carries a positive charge, chloride is excreted into the urine in equal amounts with ammonium to maintain electrical neutrality.

positive urine anion gap suggesting a kidney source of acid loss, and a negative urine anion gap is consistent with gastrointestinal bicarbonate loss.

The vomiting associated with bulimia nervosa leads to loss of gastric acid with a resulting metabolic alkalosis

Active diuretic use leads to kidney potassium wasting and a metabolic alkalosis, as does Gitelman syndrome, a defect that mimics the clinical picture of thiazide diuretic use.

Type 1 (hypokalemic distal) renal tubular acidosis is caused by a defect in hydrogen secretion by the distal tubule and is associated with a positive urine anion gap, a high urine potassium secretion, and hypokalemia.

Patients who receive kidney transplants are at increased risk of malignancy compared with the general population, and this risk is attributable, at least in part, to the effects of immunosuppressive medications.

Kidney transplant patients are at particularly high risk for squamous cell carcinomas (SCC) of the skin

SCC is more common than basal cell carcinoma and accounts for approximately 90% of skin cancers in organ recipients.

patient's baseline estimated glomerular filtration rate (eGFR) is considered the strongest predictor of the development of acute kidney injury (AKI) in the perioperative period.

An elevated preoperative serum creatinine level and the presence of chronic kidney disease (CKD) are the strongest nonmodifiable predictors of the development of AKI after cardiac surgery.

Other nonmodifiable risk factors for post–cardiac surgery AKI include advanced age, female gender, reduced left ventricular function or the presence of heart failure, insulin-dependent diabetes mellitus, peripheral vascular disease, and COPD.

Hypertension has not been shown to be a strong predictor for the development of AKI post–cardiac surgery.

Lisinopril and simvastatin have not been established as medications that increase the risk of AKI post–cardiac surgery.

Oncogenic osteomalacia is characterized by bone pain and hypophosphatemia with kidney phosphate wasting in the setting of low 1,25-dihydroxy vitamin D and normal 25-hydroxy vitamin D concentrations

Nutritional vitamin D deficiency results in low serum calcium levels and low 25-hydroxy vitamin D concentration, and it does not cause kidney phosphate wasting

Primary hyperparathyroidism is defined by an elevated parathyroid hormone level, elevated serum calcium level, and increased 1,25- dihydroxy vitamin D

The differential diagnosis of pulmonary-renal syndrome includes small-vessel vasculitis (ANCA associated), anti-GBM antibody disease (Goodpasture syndrome), and rarely, other autoimmune diseases such as cryoglobulinemic vasculitis, systemic lupus erythematosus, and IgA vasculitis.

Serologies show normal complement levels and elevated levels of anti-GBM antibodies

kidney biopsy, there is a proliferative glomerulonephritis, often with many crescents (shown, top panel). There is linear deposition of immunoglobulin along the GBM by immunofluorescence, but no electron- dense deposits on electron microscopy

Treatment is immunosuppressive therapy with cyclophosphamide and glucocorticoids, combined with daily plasmapheresis to remove circulating anti-GBM antibodies.

Membranous nephropathy is associated with the nephrotic syndrome with a low serum albumin level, which is not seen in this patient. The nephrotic syndrome alone is not typically associated with pulmonary disease, although it can be complicated with venous thromboembolic manifestations such as pulmonary embolism

Microscopic polyangiitis is the most common cause of pulmonary-renal syndrome

showing little or no immune deposits in microscopic polyangiitis (“pauci-immune glomerulonephritis”)

Trimethoprim is known to interfere with creatinine secretion without affecting the glomerular filtration rate and can cause increases in serum creatinine of up to 0.5 mg/dL (44.2 µmol/L); this rise therefore does not reflect a drop in actual kidney function.

Trimethoprim also inhibits the epithelial sodium channel in the collecting tubule, effectively acting as a potassium-sparing diuretic and potentially increasing the serum potassium level

Rifampin may cause red or orange discoloration of the urine but is not associated with a decreased GFR, an increase in serum creatinine, or hyperkalemia

Urine eosinophil testing by means of special stains has been used classically to diagnose acute interstitial nephritis, which is a diagnostic consideration in a patient taking sulfa drugs.

Ultrasonography and noncontrast helical CT of the abdomen are testing options for evaluation of suspected nephrolithiasis; CT is indicated if initial ultrasound testing is negative in a patient with a high clinical suspicion for kidney stones.

the absence of hydronephrosis on ultrasound does not rule out nephrolithiasis

In patients with AKI and oliguria, the fractional excretion of sodium (FENa) may be helpful in differentiating between prerenal AKI and AKI from renal tubular cell damage or acute tubular necrosis (ATN).

FENa measures the percent of filtered sodium excreted in the urine and is calculated as (USodium × PCr)/(UCr× PSodium) × 100. It is considered a more accurate measurement of kidney sodium avidity in prerenal states than the urine sodium concentration

FENa is less reliable when diuretics are being used because the urine sodium may not accurately reflect attempts by the kidney to retain sodium

FENa is less reliable to differentiate between prerenal and ATN if the patient use diuretics , so better to use FEUrea which is not affected by diuretics

Most patients with class III lupus nephritis and all patients with class IV lupus nephritis benefit from aggressive combination immunosuppressive therap

Patients with class I or II LN may have minimal or no kidney findings, and those with classes III and IV present with varying degrees of the nephritic syndrome. Patients with class V LN present predominantly with proteinuria. Class VI is the end stage of long-standing LN.

Class IV LN represents diffuse glomerular involvement and is the most common and severe form of nephritis associated with lupus. It is also associated with elevated anti–double stranded DNA antibody levels and hypocomplementemia, particularly during periods of active disease.

The optimal initial therapy is to increase glucocorticoid doses (typically an intravenous pulse followed by a tapering oral dose), which is accompanied by either intravenous cyclophosphamide or mycophenolate mofetil

The addition of plasmapheresis to immunosuppressive therapy has not been shown to improve outcomes in patients with LN.

treatment goal of <150/90 mm Hg for patients with hypertension who are ≥60 years

infection-related glomerulonephritis (IRGN) following a streptococcal infection. Supportive evidence includes preceding symptoms of an upper respiratory tract infection suggestive of streptococci (rapid streptococcal antigen test is positive and antistreptolysin O antibodies are elevated), followed by the nephritic syndrome in 1 week, and low C3 levels with normal C4 levels (suggesting an alternative pathway of complement activation, which is typical of IRGN).