Renal Flashcards

1
Q

renal

A

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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2
Q

renal

A

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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3
Q

renal

A

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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4
Q

renal

A

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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5
Q

rena;

A

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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6
Q

rena;

A

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

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7
Q

Renal

A

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
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8
Q

renal

A

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

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9
Q

renal

A

Treatuing high oxalater stones

  • Avoid low calcium diet
  • Reduce oxalate containing foods,
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10
Q

renal

A

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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11
Q

renal

A

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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12
Q

renal

A

RTA
NAGMA is either diarrhea or RTA

RTA should be suspected with high Cl levels with no GI losses

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13
Q

renal

A

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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14
Q

renal

A

Potassium citrate can be used to help prevent calcium oxalate stones in patients with chronic diarrhea and malabsorption.

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15
Q

RENAL

A

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

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16
Q

Renal

A

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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17
Q

rena;

A

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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18
Q

renal

A

Urine Cl is low is volume deplete states// vomiting, diarrhra

if urine cl is highm, most likely hyperaldo

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19
Q

renal

A

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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20
Q

renal

A

urine sodium less than 20 = volume depletion

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21
Q

renal

A

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.

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22
Q

RENAL

A

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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23
Q

renal

A

A diagnosis of multiple myeloma is suggested by the constellation of anemia, hypercalcemia, normal anion gap metabolic acidosis, and acute kidney injury.

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24
Q
A

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

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25
Q

renal

A

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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26
Q

renal

A

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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27
Q

renal

A

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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28
Q

renal

A

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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29
Q

renal

A

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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30
Q

renal

A

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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31
Q

renal

A

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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32
Q

renal

A

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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33
Q

renal

A

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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34
Q

renal

A

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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35
Q

renal

A

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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36
Q

renal

A

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.

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37
Q

RENAL

A

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.

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38
Q

RENAL

A

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.

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39
Q

RENAL

A

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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40
Q

RENAL

A

Screening for intracranial cerebral aneurysms using CT or MR angiography is recommended for patients with autosomal dominant polycystic kidney disease.

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41
Q

RENAL

A

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.

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42
Q

RENAL

A

In most patients with renal artery stenosis, the primary therapeutic intervention is medical management, including correction of modifiable cardiovascular risk factors.

Patients who may benefit from percutaneous angioplasty and stenting or surgical intervention include those who present with a short hypertension duration; fail medical therapy; or have severe hypertension or recurrent flash pulmonary edema, refractory heart failure, acute kidney injury following treatment with an ACE inhibitor or ARB, or progressive impaired kidney function

43
Q

RENAL

A

Intravenous isotonic fluids are the mainstay in preventing contrast-induced nephropathy.

44
Q

renal

A

Type 1 (hypokalemic distal) renal tubular acidosis is due to a defect in urine acidification in the distal nephron and is characterized by a normal anion gap metabolic acidosis, positive urine anion gap, inability to acidify urine below a pH of 6.0, and potassium wasting.

Type 2 (proximal) RTA involves a proximal tubular defect in reclaiming bicarbonate and is characterized by a normal anion gap metabolic acidosis, hypokalemia, glycosuria (without hyperglycemia), ph less than 5.5

Type 4 (hyperkalemic distal) RTA due to aldosterone deficiency or resistance is associated with hyperkalemia and a urine pH <5.5, neither of which is seen in this patient.

45
Q

renal

A

When oral loop diuretics have been maximally uptitrated, and weight loss and edema control are insufficient, it is often necessary to add a second oral diuretic (a thiazide diuretic and/or potassium-sparing diuretic) that works distal to the loop of Henle, which in this case can be accomplished via the addition of metolazone in this patient taking maximal-dose furosemide.

46
Q

renal

A

The nephrotic syndrome can be complicated by clotting manifestations due to a secondary hypercoagulable state, and risk is related to the degree of hypoalbuminemia.

Of all the nephrotic syndromes, membranous glomerulopathy carries the greatest risk for clotting abnormalities, with some series reporting thrombotic complications in up to 35% of the most severe membranous glomerulopathy cases.

47
Q

renal

A

An ACE inhibitor or angiotensin receptor blocker is an agent of choice for treatment of hypertension in a patient with chronic kidney disease.

Several studies have shown that use of an ARB or ACE inhibitor can result in decreased progression of albuminuria and CKD. Addition of losartan will also likely increase his serum potassium back to within normal range.

48
Q

renal

A

Preeclampsia is defined by new-onset hypertension and proteinuria that occurs after 20 weeks of pregnancy; new-onset hypertension with new-onset end-organ damage (such as liver or kidney injury, pulmonary edema, cerebral or visual symptoms, or thrombocytopenia) are also diagnostic.

Chronic hypertension is defined as a systolic blood pressure ≥140 mm Hg or diastolic pressure ≥90 mm Hg starting before pregnancy or before 20 weeks of gestation

Eclampsia is the presence of generalized tonic-clonic seizures in women with preeclampsia,

Preeclampsia is defined by new-onset hypertension and proteinuria (≥300 mg/24 h from a timed collection or ≥300 mg/g by urine protein-creatinine ratio) that occurs after 20 weeks of pregnancy.

49
Q

renal

A

In addition to starting antibiotics, stone removal should be considered to decrease future episodes of urinary tract infections in this patient who has a struvite stone.

50
Q

renal

A

Adynamic bone disease can occur in patients with chronic kidney disease or those on dialysis and is associated with fracture or bone pain; parathyroid hormone and alkaline phosphatase levels are typically normal.

Treatment is targeted at factors that allow PTH secretion to rise. This includes avoiding calcium-based binders, conservative use of vitamin D, and decreasing the dialysate calcium concentration

51
Q

renal

A

β2-Microglobulin–associated amyloidosis is usually seen in patients who have been on dialysis for at least 5 years. This disorder involves osteoarticular sites, and patients may present with carpal tunnel syndrome or shoulder pain. Bone cysts may be visible on radiograph.

Osteitis fibrosa cystica is the classic pathology associated with kidney disease. This disorder is associated with increased bone turnover and elevated PTH and alkaline phosphatase levels.

Osteomalacia refers to a defect with both low turnover and abnormal mineralization of bone.

52
Q

renal

A

All patients with chronic kidney disease and anemia should have iron profiles assessed, including transferrin saturation and ferritin levels; treatment target levels are a transferrin saturation level >30% and a serum ferritin level >500 ng/mL (500 µg/L) using either oral or intravenous iron supplementation.

53
Q

renal

A

The patient presents with a triad of resistant hypertension, metabolic alkalosis, and hypokalemia following the addition of a thiazide diuretic, which raises suspicion for primary hyperaldosteronism.

Testing for primary hyperaldosteronism is recommended if any of the following are present: resistant hypertension, hypokalemia (spontaneous or substantial, if diuretic induced), incidentally discovered adrenal mass, family history of early-onset hypertension, or stroke at age <40 years. Diuretics should be discontinued prior to testing to assure euvolemia.

54
Q

renal

A

Saline-responsive metabolic alkalosis typically presents with hypovolemia and a low urine chloride of <15 mEq/L (15 mmol/L); the most common causes are vomiting, nasogastric suction, and diuretic use.

55
Q

RENAL

A

Tubulointerstitial nephritis is the most common kidney manifestation of IgG4-related disease and typically presents with pyuria, proteinuria, and elevated serum IgG and IgE levels; kidney imaging may show enlarged kidneys or renal masses.

Other manifestations can include autoimmune pancreatitis, allergic rhinitis, submandibular gland swelling, an elevated antinuclear antibody (ANA) titer, low serum complement levels, elevated serum IgG, elevated serum IgE, and peripheral eosinophilia. Kidney imaging may show enlarged kidneys or renal masses that may present as small peripheral cortical nodules. Th

56
Q

RENAL

A

Although Sjögren syndrome can affect lacrimal and salivary glands and cause TIN, this patient’s constellation of symptoms is more consistent with IgG4-related disease. Dryness of the eyes and mouth is extremely common in Sjögren but not in IgG4-related disease.

57
Q

RENAL

A

In patients with chronic kidney disease, NSAIDs are potentially nephrotoxic and a frequent cause of acute kidney injury and should be avoided.

58
Q

RENAL

A

Treatment using thiazide diuretics is appropriate for calcineurin inhibitor–induced hypertension and hyperkalemia in kidney transplant recipients.

Patients with kidney transplants must receive immunosuppressive medications to prevent their immune system from rejecting the kidney allograft. Doses are typically highest immediately after transplant and are tapered gradually over several months to minimize toxicities associated with these medications while maintaining adequate immunosuppression. The most commonly used immunosuppressants in the immediate posttransplant period for immunosuppression induction are anti–T-cell and interleukin-2 receptor–blocking antibodies. The most commonly prescribed medications for chronic maintenance immunosuppression include calcineurin inhibitors (tacrolimus or cyclosporine), antimetabolites (mycophenolate mofetil or azathioprine), and glucocorticoids. Although these medications are usually well tolerated, they can have significant side effects. Calcineurin inhibitors activate the sodium chloride cotransporter in the distal convoluted tubule, which reabsorbs sodium and chloride to cause hypertension.

59
Q

RENAL

A

Management of hypermagnesemia includes discontinuation of magnesium-containing medications, administration of saline diuresis to enhance magnesium excretion, and administration of intravenous calcium to treat severe symptoms.

Hypermagnesemia is usually not associated with significant symptoms until the level is >7.2 mg/dL (2.9 mmol/L). Symptoms include somnolence, headache, loss of deep tendon reflexes, bradycardia, hypotension, and hypocalcemia. At levels >12 mg/dL (4.9 mmol/L), flaccid paralysis, respiratory failure, and complete heart block can occur.

In patients with hypotension and significant neuromuscular deficits, treatment is aimed at direct antagonism of the effects of hypermagnesemia, which is accomplished by intravenous administration of calcium

60
Q

RENAL

A

Suspected masked hypertension (defined as blood pressure that is normal in the office but elevated in the ambulatory setting) should be confirmed with ambulatory blood pressure monitoring or home blood pressure monitoring.

61
Q

RENAL

A

Initial antihypertensive treatment in black patients without chronic kidney disease should include a thiazide diuretic or calcium channel blocker, or combination of the two.

62
Q

RENAL

A

The American College of Obstetricians and Gynecologists defines chronic hypertension as a systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mm Hg starting before pregnancy or before 20 weeks of gestation or persists longer than 12 weeks’ postpartum.

Gestational hypertension first manifests after 20 weeks of pregnancy without proteinuria or other end-organ damage and resolves within 12 weeks of delivery.

63
Q
A

Serologic testing for anti–glomerular basement membrane antibodies and kidney biopsy can confirm the diagnosis of anti–glomerular basement membrane antibody disease as the cause of rapidly progressive glomerulonephritis.

64
Q

RENAL

A

In the setting of anuric-oliguric acute kidney injury, intermittent hemodialysis allows for rapid correction of electrolyte disturbances and rapid removal of drugs or toxins.

This patient has severe hyperkalemia with electrocardiographic changes, which should be corrected urgently to prevent lethal cardiac arrhythmias. Calcium, insulin, and dextrose are only temporizing measures and will not result in potassium removal from the body. Only dialysis will result in potassium removal from the body.

65
Q

RENAL

A

Type 4 (hyperkalemic distal) renal tubular acidosis is characterized by hyperkalemia, a normal anion gap metabolic acidosis, impaired urine acidification (positive urine anion gap), and a urine pH <5.5.

66
Q

RENAL

A

The presence of hematuria, dysmorphic erythrocytes, and proteinuria in a patient with known systemic lupus erythematosus (SLE) is highly suggestive of lupus nephritis;

A kidney biopsy should be performed in patients with known systemic lupus erythematosus with suspected significant kidney involvement to establish the diagnosis and to identify the class, which will guide treatment decisions.

67
Q

RENAL

A

a proliferative lupus nephritis (class III or IV), in which case treatment with glucocorticoids and mycophenolate mofetil or cyclophosphamide would be indicated (mycophenolate mofetil would likely be preferred given this patient’s age

68
Q

RENAL

A

Peripherally inserted central catheter placement before or after hemodialysis initiation is associated with adverse vascular access outcomes in patients with chronic kidney disease.

A tunneled internal jugular central venous catheter is the most appropriate venous access strategy for this patient. In patients with osteomyelitis, 6 weeks of antimicrobial therapy after surgical débridement is the preferred treatment course, and for most patients this requires long-term reliable venous access. However, this patient’s advanced degree of kidney disease, relatively young age, and type 2 diabetes mellitus put her at high risk for progressing to end-stage kidney disease, and the upper extremity veins should be protected for future hemodialysis access creation

69
Q

RENAL

A

An ACE inhibitor or angiotensin receptor blocker is the initial treatment of choice for hypertension in patients with diabetes mellitus and albuminuria.

70
Q

RENAL

A

Some medications (such as cimetidine, trimethoprim, cobicistat, dolutegravir, bictegravir, and rilpivirine) reduce proximal tubule secretion of creatinine, resulting in increases in serum creatinine that are nonprogressive; repeat serum creatinine measurement is required to confirm stable levels.

71
Q

RENAL

A

Topiramate, a carbonic anhydrase inhibitor, causes a decrease in urinary citrate excretion and formation of alkaline urine that favor the creation of calcium phosphate stones.

72
Q

RENAL

A

Chronic tubulointerstitial nephritis can be caused by proton pump inhibitors, and the median time from drug initiation to diagnosis may exceed 6 to 9 months.

73
Q

RENAL

A

The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend consideration of erythropoiesis-stimulating agents to treat anemia in patients with chronic kidney disease and adequate iron stores who have hemoglobin concentrations <10 g/dL (100 g/L); the dose should be titrated to avoid hemoglobin concentrations increasing above 11.5 g/dL (115 g/L).

74
Q

RENAL

A

In patients with poststreptococcal glomerulonephritis (group A Streptococcus, or Streptococcus pyogenes), there is a latent period between the resolution of the streptococcal infection and the acute onset of the nephritic syndrome, usually 7 to 10 days after oropharyngeal infections and 2 to 4 weeks after skin infections. In adults with non-poststreptococcal IRGN, the glomerulonephritis often coexists with the triggering infection.

In adults, most cases of infection-related glomerulonephritis are no longer poststreptococcal, and the glomerulonephritis often coexists with the triggering infection.

75
Q

renal

A

Based on evidence that the greatest absolute benefit of antihypertensive therapy is seen in patients with the highest blood pressure and cardiovascular risk, the American College of Physicians and American Academy of Family Physicians recommend that antihypertensive drugs be initiated in patients ≥60 years old if blood pressure is >150/90 mm Hg, with a goal of reducing systolic blood pressure to <150 mm Hg; the American College of Cardiology/American Heart Association recommends a systolic blood pressure target of <130 mm Hg in patients ≥65 years old.

76
Q

RENAL

A

Initial treatment of secondary hyperparathyroidism in chronic kidney disease stages G3 through G5 is correction of serum calcium, phosphorus, and vitamin D levels.

Sevelamer is the most appropriate treatment for this patient with secondary hyperparathyroidism and hyperphosphatemia associated with stage G4 chronic kidney disease (CKD).

calcitriol may be warranted if hyperparathyroidism persists after normalization of serum calcium and phosphorus levels even in the setting of normal 25-hydroxyvitamin D levels, as impaired hydroxylation at the 1 position by the kidney can lead to functional deficiency.

77
Q

RENAL

A

Many medications, such as NSAIDS, can result in reversible elevations in blood pressure; discontinuation of the drug and a reassessment of blood pressure 1 month later are necessary to confirm a return to normal blood pressure measurement.

78
Q

RENAL

A

Hepatitis B virus infection and HIV infection have been linked to glomerular diseases, but these are classically associated with the nephrotic syndrome, specifically membranous glomerulopathy with hepatitis B virus infection and focal segmental glomerulosclerosis with HIV infection.

An immune-complex membranoproliferative glomerulonephritis is the classic form of kidney involvement seen in patients with hepatitis C virus infection.

The more common pattern is immune-complex deposition with the presence of both immunoglobulin (IgG, IgM, and/or IgA) and complement (C1q and/or C3) on immunofluorescence, which infers that the classical pathway has been activated by an inciting cause or event that generally falls into one of three major categories: infectious, autoimmune, or malignancy associated.

79
Q

RENAL

A

Lead nephropathy can occur in patients with occupational exposure to lead or exposure to lead in water, soil, paint, or food products; it is frequently associated with hyperuricemia, hypertension, and recurrent gouty attacks.

Cadmium nephropathy occurs in patients with prolonged exposure to plastic, metal, alloys, and electrical equipment manufacturing industries.

80
Q

RENAL

A

Lead nephropathy can occur in patients with occupational exposure to lead or exposure to lead in water, soil, paint, or food products; it is frequently associated with hyperuricemia, hypertension, and recurrent gouty attacks.

Cadmium nephropathy occurs in patients with prolonged exposure to plastic, metal, alloys, and electrical equipment manufacturing industries.

81
Q
A

The normal physiologic response to systemic acidosis is an increase in urine acid excretion. Therefore, an initial diagnostic step in normal anion gap metabolic acidosis is to determine whether the kidney is appropriately excreting acid or whether impaired kidney acid excretion is the cause of the metabolic acidosis. Increased acid excretion by the kidney is reflected as a marked increase in urine ammonium. However, urine ammonium is difficult to measure directly. Because ammonium carries a positive charge, chloride is excreted into the urine in equal amounts with ammonium to maintain electrical neutrality. Therefore, the amount of chloride in the urine reflects the amount of ammonium present, and the urine anion gap can be used as an indicator of the ability of the kidney to excrete acid. The urine anion gap is calculated as follows:

82
Q

RENAL

A

NEGUTIVE neGUTive UAG means its GI

Urine sodium + urine K - Urine Cl

83
Q

renal

A

Kidney biopsy should be considered in patients with acute kidney injury from no apparent or unclear cause, suspected glomerulonephritis, or unexplained systemic disease.

ostrenal AKI results from urinary tract obstruction. Bladder outlet obstruction should be suspected in patients with prostate enlargement or in the setting of diabetes mellitus (neurogenic bladder), pain medications, or anticholinergic medications.

84
Q

renal

A

Genetic counseling potentially followed by genetic testing for hereditary nephritis (Alport syndrome) is appropriate for this patient. Hereditary nephritis is a familial form of glomerulonephritis that affects approximately 0.4% of U.S. adults. The earliest presentation is microscopic hematuria, with or without proteinuria

85
Q

renal

A

Calcium oxylate vs calcium phosphate stones

Oxylylate = diarrhea - crohns- GI issues
Patients with diarrhea who are volume depleted and have a metabolic acidosis are at increased risk for developing kidney stones, particularly calcium oxalate stones and, less commonly, uric acid stones.

86
Q

renal

A

D-lactic acidosis is characterized by an increased anion gap metabolic acidosis in patients with short-bowel syndrome or other forms of malabsorption; diagnosis is confirmed by measuring the D-lactate level rather than the conventional L-lactate level.

Ethylene glycol or methanol intoxication also presents with an increased anion gap metabolic acidosis and neurologic symptoms. However, they are usually accompanied by a serum osmolal gap >10 mOsm/kg H2O (6 mOsm/kg H2O in this case) and a serum bicarbonate level <10 m

87
Q

renal

A

Pyroglutamic acidosis also manifests as mental status changes in the context of an increased anion gap. This acidosis occurs in patients chronically receiving therapeutic doses of acetaminophen. Susceptible patients are those with critical illness, poor nutrition, liver disease, and chronic kidney disease, as well as those on a strict vegetarian diet. Diagnosis can be confirmed by measuring urine levels of pyroglutamic acid.

88
Q

renal

A

The renin-angiotensin system agents (ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors) are contraindicated in pregnancy and should be stopped prior to conception.

This patient’s blood pressure is well below this goal of therapy, and her blood pressure would be expected to decline during pregnancy. Therefore, monitoring her blood pressure after discontinuation of losartan is a reasonable approach. If her blood pressure rises, initiation of a drug that is safe during pregnancy is recommended. Candidate drugs include methyldopa, nifedipine, and/or labetalol.

89
Q

renal

A

Hypertension is common in patients with autosomal dominant polycystic kidney disease (ADPKD), often preceding chronic kidney disease; kidney ultrasonography is the most common and least costly screening and diagnostic method for ADPKD.

90
Q

renal

A

In kidney transplant recipients who are planning pregnancy, mycophenolate mofetil, sirolimus, and everolimus must be discontinued 3 to 6 months prior to conception and replaced with azathioprine, which is generally safer and well tolerated in pregnancy.

Kidney transplant recipients should wait 1 to 2 years with a stable allograft before attempting conception.

91
Q

renal

A

Mycophenolate mofetil (as well as sirolimus and everolimus) is teratogenic and needs to be replaced 3 to 6 months prior to conception with azathioprine, which is generally safer and well tolerated in pregnancy.

Calcineurin inhibitors (both tacrolimus and cyclosporine) have been used safely in pregnancy

92
Q

renal

A

Clinical clues to the diagnosis of light chain cast nephropathy from multiple myeloma include an elevated urine protein-creatinine ratio with minimal proteinuria by urine dipstick, anemia, and hypercalcemia.

93
Q

renal

A

Lupus nephritis and postinfectious glomerulonephritis can present with macroscopic glomerular hematuria, but these disease states usually induce low complement levels (low C3 with or without low C4). Postinfectious glomerulonephritis, when associated with upper respiratory infections caused by streptococcal organisms, usually occurs 2 to 3 weeks after the resolution of the streptococcal infection.

94
Q

renal

A

Referral for kidney transplant evaluation is indicated when the estimated glomerular filtration rate is <30 mL/min/1.73 m2 to allow for adequate time to identify suitable living donors or to be put on an early listing if no living donor is available.

95
Q

renal

A

Vasoconstrictor therapy with octreotide and oral midodrine is appropriate for this patient with type 1 hepatorenal syndrome (HRS).

Dialysis should be initiated only if the patient does not respond to HRS medical therapy with midodrine and octreotide and/or if indications for dialysis develop. Absolute indications for dialysis include hyperkalemia, metabolic acidosis, and pulmonary edema refractory to medical therapy; uremic symptoms; uremic pericarditis; and certain drug intoxications.

96
Q

renal

A

Urea osmotic diuresis is the most likely cause of this patient’s hypernatremia. This patient is recovering from acute kidney injury and is having a urea diuresis, with an elevated urine osmolality of 420 mOsm/kg H2O. In osmotic diuresis, urine osmolality is usually between 300 and 600 mOsm/kg H2O. The majority of the osmolality of the urine is made up of nonelectrolytes. This loss of electrolyte-free water is causing her serum sodium level to increase. The two major nonelectrolytes found in urine are urea and glucose. Her glucose is only 136 mg/dL (7.5 mmol/L), below the threshold for glucose appearing in the urine; therefore, the likely cause is excretion of urea. This can be confirmed by measuring urea in the urine.

97
Q

renal

A

Indications for kidney biopsy include glomerular hematuria, severely increased albuminuria, acute or chronic kidney disease of unclear cause, and kidney transplant dysfunction or monitoring.

98
Q

renal

A

Non-dialytic therapy is a reasonable treatment option for elderly patients with end-stage kidney disease and multiple comorbidities; treatment focuses on symptom management.

99
Q

renal

A

Although thiazide diuretics are frequently used as initial diuretic therapy, they are generally less effective in patients with lower glomerular filtration rates. At estimated glomerular filtration rates <30 mL/min/1.73 m2, loop diuretics tend to be more effective at controlling extracellular volume expansion and should be used instead of (or added to) thiazide diuretics.

100
Q

renal

A

Cisplatin-induced acute kidney injury is characterized by polyuria, tubular injury, hypomagnesemia, and proximal renal tubular acidosis with Fanconi syndrome.

101
Q

renal

A

The kidney failure risk equation uses four variables (age, sex, estimated glomerular filtration rate, and albuminuria) to predict 2-year and 5-year risk of end-stage kidney disease in patients with stages G3 to G5 chronic kidney disease.

102
Q

renal

A

AA amyloid is formed by serum amyloid A protein, an acute phase reactant produced in various inflammatory diseases such as rheumatoid arthritis; confirmation of AA renal amyloidosis requires a kidney biopsy.

Chronic inflammatory states, particularly rheumatoid arthritis, are associated with production of amyloid protein
LOOK FOR HEART Faliure too

Confirmation would therefore require a kidney biopsy in this case. Current treatment strategies are aimed at the underlying disease. Tocilizumab, an anti–interleukin-6 antibody, has been used successfully in patients with AA amyloidosis from rheumatoid arthritis.

103
Q

RENAL

A

Patients with end-stage kidney disease have a markedly increased risk for renal cell carcinoma, and a high level of suspicion is warranted in patients with symptoms such as new-onset gross hematuria or unexplained flank pain.

Patients with ESKD have a markedly increased risk for renal cell carcinoma. Although current guidelines do not support routine screening for renal cell carcinoma in all patients with CKD, a high level of suspicion is warranted in patients with symptoms such as new-onset gross hematuria or unexplained flank pain.

104
Q

RENAL

A

There is no benefit in starting renal replacement therapy (RRT) in asymptomatic patients or at an arbitrary estimated glomerular filtration rate cutoff compared with careful clinical management and initiating RRT for symptoms or metabolic abnormalities that are refractory to medical treatment.