Renal Flashcards
renal
The maximal daily recommended dose for hydrochlorothiazide is 25 mg for the treatment of hypertension; side effects increase beyond this dose with little further antihypertensive effect.
Additional evidence of overtreatment includes an increase in his serum creatinine level, hyponatremia, hypokalemia, and the development of metabolic alkalosis.
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A kidney biopsy is required to make the diagnosis of glomerulopathy associated with the nephrotic syndrome in adult patients.
MCG is the cause of the nephrotic syndrome in 10% to 15% of adults, with a significantly higher incidence in elderly patients (≥65 years of age) and very elderly patients (≥80 years of age). Most cases are idiopathic, but secondary causes must be considered in adults, including medications such as NSAIDs.
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The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend treatment of metabolic acidosis with alkali therapy in patients with chronic kidney disease when the serum bicarbonate is chronically <22 mEq/L (22 mmol/L).
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Glucocorticoids are first-line therapy for primary minimal change glomerulopathy; standard treatment of the nephrotic syndrome (ACE inhibitor or angiotensin receptor blocker, diuretics for edema, and cholesterol-lowering medication if total cholesterol >200 mg/dL [5.1 mmol/L]) is also indicated as needed.
Diuretics plus high-dose prednisone is the most appropriate treatment for this patient with minimal change glomerulopathy
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Glomerular diseases with low complement
- post infections GN
- Lupus nephreitis
- infective endocardit
- Cryoglobune mia0 addosictaed iwith hep c
- membranoprolifer- GN- Associated with Hep b and C
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both occur after URI
with iga nephroparthy, complment levels are NORMAL
WIht post infectious GN, there i sLOW completment and it stakes 7 to 10 dayd
Renal
multiple myloema and amylofiss
- if there is a discrepancy betweeb urine dipsticl and urine cr ratio, consider that free light chains may be accountiung for the difference
renal
Calcium oxalate is the most common form of kidney stone
Think rta if calcium phopsahe stone
Citrate inhibit stone from forming
Calcium, oxalate and uric acid, increase stone formation
High calcium WORST risk factor . Treat with HCTZ, Chlorthalidone,
REDUCE animal protein intake, reducne Na, reducse cucrose and fructose
renal
Treatuing high oxalater stones
- Avoid low calcium diet
- Reduce oxalate containing foods,
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Uric acid stones
- acidic urine ph
- give potassium citrate to increase urine ph (means you have low citrate in the urine)
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Antiproteinuric therapy with an ACE inhibitor or angiotensin receptor blocker is the hallmark and most validated treatment strategy for IgA nephropathy.
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RTA
NAGMA is either diarrhea or RTA
RTA should be suspected with high Cl levels with no GI losses
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NAGMA
Urine anion gap
- Urine Na, K, Cl
- If urine AG is negative, diarrhea
- If urine AG is positive, Typ1 1 RTA (This has high urine cl becaise ut cant be excreted and tha means you have issues with RTA
type 1 rta has low k
typw 2 has low k and negative AG
Type 4 RTA has hyper k
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Potassium citrate can be used to help prevent calcium oxalate stones in patients with chronic diarrhea and malabsorption.
RENAL
The best predictors for the presence of diabetic nephropathy are duration of diabetes mellitus for more than 8 years followed by the presence of the nephrotic syndrome.
The addition of an ACE inhibitor or angiotensin receptor blocker (ARB) is the most appropriate management for this patient with diabetic nephropathy
Renal
Initial management of rhabdomyolysis-induced acute kidney injury includes aggressive fluid resuscitation with normal saline aimed at maintaining a urine output of 200 to 300 mL/h.
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Intravenous volume expansion with isotonic crystalloids has been shown to decrease the incidence of contrast-induced nephropathy in patients at risk.
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Urine Cl is low is volume deplete states// vomiting, diarrhra
if urine cl is highm, most likely hyperaldo
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anytine you have a hypeetensive patient with a low k and high bicarb, think to check renin aldo, think secondary causes
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urine sodium less than 20 = volume depletion
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Differentiate siadh from psychogenic (both are euvolemic with urine Na OVER 20)
In SIADH, Urine osmolality is HIGH because ADH is present
In psychogenic, urine osmolality should be LOW
Urine osmolality <100 mOsm/kg H2O indicates excessive water intake, as seen with psychogenic polydipsia or poor solute intake.
RENAL
Hypernatremia
If urine osm is high, could be water deprivation
If urine osm is low, could be cenotral vs nephorgenivc DI
Central DI will respond to desmopresssin
Nepgrohegnic wont respoind to Desmopressin, treat with thiazode
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A diagnosis of multiple myeloma is suggested by the constellation of anemia, hypercalcemia, normal anion gap metabolic acidosis, and acute kidney injury.
This patient has typical findings of ethylene glycol toxicity, including central nervous system depression, an increased anion gap metabolic acidosis, and an increased osmolal gap.
In patients with an increased anion gap acidosis, calculation of the serum osmolal gap is helpful in assessing the presence of unmeasured solutes, such as ingestion of certain toxins (for example, methanol or ethylene glycol). The serum osmolal gap is the difference between the measured and calculated serum osmolality. Serum osmolality can be calculated using the following formula:
When the measured osmolality exceeds the calculated osmolality by >10 mOsm/kg H2O, the osmolal gap is considered elevated.
thylene glycol intoxication may take days, empiric therapy with fomepizole and aggressive fluid resuscitation with crystalloids (250-500 mL/h intravenous initially) s
renal
Hypoaldosteronism caused by heparin, inhibitors of the renin-angiotensin system, type 4 renal tubular acidosis, or primary adrenal disease can cause hyperkalemia, especially in patients with chronic kidney disease or diabetes mellitus, or in those taking an ACE inhibitor or angiotensin receptor blocker.
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ANCA-associated glomerulonephritis is typically characterized by a vasculitic prodrome of malaise, arthralgia, myalgia, and skin findings; hematuria, proteinuria, and acute kidney injury are present, and kidney biopsy will confirm diagnosis.
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Pyroglutamic acidosis occurs in patients receiving therapeutic doses of acetaminophen on a chronic basis in the setting of critical illness, poor nutrition, liver disease, chronic kidney disease, or a strict vegetarian diet; diagnosis can be confirmed by measuring urine levels of pyroglutamic acid.
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D-Lactic acidosis presents with an increased anion gap metabolic acidosis and characteristic neurologic findings of intermittent confusion, slurred speech, and ataxia in patients with short-bowel syndrome. Accumulation of the D-isomer of lactate can occur in patients with short-bowel syndrome following jejunoileal bypass or small-bowel resection. In these patients, excess carbohydrates that reach the colon are metabolized to D-lactate. Laboratory studies show increased anion gap metabolic acidosis with normal plasma lactate levels, because the D-isomer is not measured by conventional laboratory assays for lactate. Diagnosis is confirmed by specifically measuring D-lactate. This patient’s lack of short-bowel syndrome rules out this diagnosis.
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Abdominal compartment syndrome is defined as a sustained intra-abdominal pressure >20 mm Hg associated with at least one organ dysfunction; management includes supportive therapy, abdominal compartment decompression, and correction of positive fluid balance.
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Patients with nonglomerular hematuria should be stratified as high, intermediate, or low risk for urothelial cancer using factors that include age, gender, tobacco use, extent of hematuria, exposure to urothelial carcinogens, or chronic irritative voiding symptoms; intermediate- or high-risk patients require imaging of the genitourinary tract and cystoscopy.
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Risk factors associated with vancomycin nephrotoxicity include chronic kidney disease, prolonged therapy, doses ≥4 g/d, trough concentrations >15 mg/L, and concomitant use of loop diuretics.
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Treatment of acute symptomatic hyponatremia includes a 100-mL bolus of 3% saline to increase the serum sodium level by 2 to 3 mEq/L (2-3 mmol/L).
Acute hyponatremia is associated with an increase in brain water and cerebral edema and should be treated rapidly. Because the brain has not adapted to the hypotonic environment by the release of organic osmolytes, the risk of rapid correction and development of osmotic demyelination is absent.
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Renal artery imaging is the most appropriate diagnostic test to perform next to evaluate for fibromuscular dysplasia in this young woman with new-onset hypertension.
The elevation of serum creatinine more than 30% from baseline after the initiation of an ACE inhibitor is a clue that renovascular hypertension may be present. Fibromuscular dysplasia is associated with aneurysm and/or dissection in a variety of vascular territories (for example, renal artery, carotid artery, and intracranial arteries).
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Only 50% of stones >6 mm will pass spontaneously, whereas stones >10 mm are extremely unlikely to pass spontaneously. Urologic intervention is required in all patients with evidence of infection, acute kidney injury, intractable nausea or pain, and stones that fail to pass or are unlikely to pass.
Medical expulsive therapy with α-blocker therapy (such as tamsulosin) or a calcium channel blocker (such as nifedipine) can aid the passage of small stones (≤10 mm in diameter).
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Kidney involvement in sarcoidosis can manifest as nephrocalcinosis from hypercalcemia and hypercalciuria, and as tubulointerstitial nephritis with granuloma formation.
Hypercalcemia occurs due to peripheral conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D by activated macrophages. Parathyroid hormone is typically suppressed in response to the hypercalcemia.
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The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend treatment of dyslipidemia with a statin in patients aged ≥50 years with an estimated glomerular filtration rate <60 mL/min/1.73 m2, but not treated with chronic dialysis or kidney transplantation.
RENAL
Noncontrast helical CT is the gold standard for diagnosis of nephrolithiasis.
MRI with contrast is not as sensitive as CT in detecting suspected kidney stones. Due to lack of radiation, MRI may be useful in pregnant women with stone disease if ultrasound is nondiagnostic.
RENAL
Cystatin C may be preferable to creatinine to assess kidney function in individuals with higher muscle mass.
Increased muscle mass can result in an increase in serum creatinine level in the absence of change in kidney function.
Cystatin C, which is cleared by the kidney, is produced by all nucleated cells; therefore, levels are less dependent on muscle mass. Cystatin C can also be used for more accurate glomerular filtration rate estimation in these patients as a component of the Chronic Kidney Disease Epidemiology Collaboration equation.
RENAL
Hypercalciuria is the most common metabolic risk factor for calcium oxalate stones.
In patients with hypercalciuria and kidney stones, calcium excretion and stone formation can be decreased by the use of thiazide diuretics.
In calcium stones that form on a uric acid nidus, allopurinol has been associated with a decrease in stone formation.
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Screening for intracranial cerebral aneurysms using CT or MR angiography is recommended for patients with autosomal dominant polycystic kidney disease.
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Patients with newly diagnosed primary membranous glomerulopathy are usually observed for 6 to 12 months while on conservative therapy (renin-angiotensin blockade, cholesterol-lowering medication, and edema management) to allow time for possible spontaneous remission before initiating immunosuppression.
Although hepatitis B and C virus infections, along with lupus, are well-known forms of secondary membranous glomerulopathy in adults, this patient’s screening tests are negative and, with PLA2R antibody positivity, further testing is unnecessary.