From KSAP
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Adrenal incidentalomas
Asymptomatic hematuria
Fractional excretion of Magnesium
Vancomycin toxicity
Asymptomatic hematuria
The finding of asymptomatic persistent and isolated hematuria of glomerular origin is typically related to one of three causes:
IgA nephropathy
Hereditary nephritis (Alport syndrome)
Thin basement membrane nephropathy
IgA nephropathy is the most common of these three and can also be familial. Patients who have IgA nephropathy without proteinuria have an excellent prognosis, and no therapy is indicated so periodic evaluation is appropriate.
Women with X-linked Alport syndrome have a better prognosis than men but a significant number can progress to proteinuria, impairment of kidney function, and ESRD. The diagnosis can be established by kidney biopsy, skin biopsy, and or by genetic testing. However, results of these tests are unlikely to alter management of this patient. Instead, the best approach is to periodically reevaluate her blood pressure, kidney function, and proteinuria. Should any abnormalities develop, a more specific diagnosis could be sought. In addition, her children should be followed closely.
Thin basement membrane nephropathy: Patients with this disorder typically have glomerular bleeding but usually have normal kidney function without proteinuria.
Vancomycin toxicity
the combination of vancomycin and piperacillin-tazobactam is associated with AKI in up to 16% patients exposed to this combination for more than 48 hours.
Adrenal incidentalomas
Incidentalomas are identified in approximately 4% of abdominal CT scans. Most adrenal nodules are non-hypersecreting adenomas, but cortisol secreting adenomas account for 5%, pheochromocytomas for 5%, and aldosterone secreting adenomas for 1%. Adrenocortical carcinoma or metastatic cancer is less common and may have other diagnostic features including mass effect, rapid change, overt signs and symptoms of steroid hormone overproduction, or features of extra-adrenal cancer.
Once identified, the adrenal incidentaloma should be evaluated for biochemical activity, guided by the clinical history and examination.
An elevated morning aldosterone-to-renin activity ratio at 20 and a plasma aldosterone concentration greater than 15 ng/dL; both suggest primary hyperaldosteronism, but confirmatory testing is recommended.Either intravenous saline suppression or 24-hour urine aldosterone after oral sodium loading can be used to confirm primary hyperaldosteronism. Once primary hyperaldosteronism is confirmed, adrenal vein sampling could be pursued to confirm that the adrenal adenoma identified on imaging is the source of the excess aldosterone. Conversely, some experts would argue that in a male patient with long-standing, stage 1 hypertension prescribed multiple medications, cure with adrenalectomy is unlikely, so management would focus on transitioning to BP control with mineralocorticoid receptor blockers. 10/19 55
Fractional excretion of Magnesium
58. The fractional excretion of magnesium is calculated as follows:
| IF: | Result | Reference range |
|---|---|---|
| Creatinine | 0.65 mg/dL | 0.5-1.1 |
| Magnesium | 1.2 mEq/L | 1.6-2.6 |
| Urine Magnesium | 1.23 mEq/L | varies |
| Urine creatinine | 100 mg/dL | varies |
| [(Urine Mag x serum Creat)/(Serum Mag x Urine Creat)]x100% | ||
| [(1.23 x 0.65)/(1.2 x 100)]x100%=0.66% |
In the setting of hypomagnesemia, renal conservation should achieve an FEMg of <2%. A FEMg of 0.66%, indicates that hypomagnesemia cannot be attributed to renal losses. 10/19 58