Lipid Profile, Serum Ceratinine, eGFR, Uric acid, Electrolytes, FBS, RBS, CBG, 2 Hours post glucose BS HBAIC Urinalysis

Question 1

is the most widely used marker for GFR, which is related directly to urine creatinine (UCr) excretion and inversely to PCr.

Answer 1

Plasma creatinine (PCr)

Question 2

Urea clearance may underestimate GFR significantly
because of urea reabsorption by the tubule. In contrast, creatinine isderived from muscle metabolism of creatine, and its generation varies little from day to day

Answer 2

Creatinine clearance (CrCl), an approximation of GFR, is measured
from plasma and urinary creatinine excretion rates for a
defined period (usually 24 h) and is expressed in milliliters per
minute: CrCl = (Uvol × UCr)/(PCr × Tmin).

Question 3

Creatinine is useful for
estimating GFR because it is a small, freely filtered solute that is
not reabsorbed by the tubules.

Answer 3

PCr levels can increase acutely from dietary ingestion of cooked meat, however, and creatinine can be
secreted into the proximal tubule through an organic cation pathway (especially in advanced progressive chronic kidney disease), leading
to overestimation of GFR.

Question 4

Cockcroft-Gault:

Answer 4

CrCl (mL/min) =

140 − age (years) × weight (kg) × [0.85 if female]
/(72 × PCr (mg/dL).

Question 5

a member of the cystatin superfamily of
cysteine protease inhibitors, is produced at a relatively constant rate from all nucleated cells. Serum cystatin C has been proposed to be a more sensitive marker of early GFR decline than is PCr; however, like
serum creatinine, cystatin C is influenced by the patient’s age, race,
and sex and also is associated with diabetes, smoking, and markers of
inflammation.

Answer 5

Cystatin C,

Question 6

Patients with advanced chronic renal insufficiency often have some

Answer 6

proteinuria, nonconcentrated urine (isosthenuria; isosmotic with plasma), and small kidneys on ultrasound, characterized by increased echogenicity
and cortical thinning.

Question 7

Decreased renal perfusion accounts for %

Answer 7

40–80% of cases of acute
renal failure and, if appropriately treated, is readily reversible. The etiologies of prerenal azotemia include any cause of decreased circulating blood volume (gastrointestinal hemorrhage, burns, diarrhea, diuretics), volume sequestration (pancreatitis, peritonitis,
rhabdomyolysis), or decreased effective arterial volume (cardiogenic shock, sepsis).

Question 8

True or “effective” arterial hypovolemia leads to a fall in

mean arterial pressure, which in turn triggers a series of neural and humoral responses,

Answer 8

including activation of the sympathetic nervous
and renin-angiotensin-aldosterone systems and antidiuretic hormone (ADH) release.

GFR is maintained by prostaglandin-mediated relaxation of afferent arterioles and angiotensin II–mediated constriction
of efferent arterioles

Blockade of prostaglandin production by NSAIDs can result in severe vasoconstriction and acute renal failure

Blocking angiotensin action with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) decreases efferent arteriolar
tone and in turn decreases glomerular capillary perfusion pressure

Question 9

Once the mean arterial pressure falls below ____

Answer 9

80 mmHg, GFR declines steeply

Question 10

Patients with bilateral renal artery stenosis (or stenosis in a solitary kidney) are dependent on

Answer 10

efferent arteriolar vasoconstriction for maintenance of glomerular filtration pressure and are particularly susceptible to a precipitous decline in GFR when given ACE inhibitors or ARBs.

Question 11

In prerenal conditions, the tubules are intact, leading to

Answer 11

a concentrated urine (>500 mosmol), avid Na retention (urine Na concentration, <20 mmol/L; fractional excretion of Na, <1%), and UCr/PCr >40

Question 12

The prerenal urine sediment is usually normal or has hyaline and granular casts, whereas the sediment of ATN is

Answer 12

ATN usually is filled with cellular debris, tubular epithelial casts, and dark (muddy brown) granular casts

Question 13

Laborat ory Findings in Acute Renal Failure

Answer 13

Prerenal Azotemia

BUN/PCr ratio >20:1
Urine sodium U Na, meq/L <20
Urine osmolality, mosmol/L H2O >500
Fractional excretion of sodiuma <1%
Urine/plasma creatinine UCr/PCr >40
Urinalysis (casts) None or hyaline/
granular

Oliguric Acute Renal Failure
BUN/PCr ratio 10–15:1
Urine sodium U Na, meq/L >40
Urine osmolality, mosmol/L H2O <350
Fractional excretion of sodiuma >2%
Urine/plasma creatinine UCr/PCr <20
Urinalysis (casts) Muddy brown

Question 14

Ischemic and toxic ATN account for %

Answer 14

~90% of cases of acute intrinsic renal failure

Ischemic ATN is observed most frequently in patients who have undergone major surgery, trauma, severe hypovolemia, overwhelming sepsis, or extensive burns.

Nephrotoxic ATN complicates the administration
of many common medications, usually by inducing a combination of intrarenal vasoconstriction, direct tubule toxicity, and/ or tubule obstruction. The kidney is vulnerable to toxic injury by virtue of its rich blood supply (25% of cardiac output) and its ability to concentrate and metabolize toxins. A diligent search for hypotension and nephrotoxins usually uncovers the specific etiology of ATN.

Urinalysis usually shows mild to moderate proteinuria, hematuria, and pyuria (~75% of cases) and occasionally WBC casts. The finding of RBC casts in interstitial nephritis has been reported but should prompt a search for glomerular diseases

Question 15

Atheroembolic renal failure can occur spontaneously but most often is associated
with recent aortic instrumentation. The emboli are cholesterol-rich and lodge in medium and small renal arteries, with a consequent

Answer 15

eosinophil-rich inflammatory reaction. Patients with atheroembolic
acute renal failure often have a normal urinalysis, but the urine may
contain eosinophils and casts

Question 16

Oliguria refers to a 24-h urine output

Answer 16

<400 mL,

and anuria isthe complete absence of urine formation (<100 mL)

Nonoliguria refers to urine output >400 mL/d
in patients with acute or chronic azotemia.

Question 17

The dipstick measurement detects only

Answer 17

albumin and givesfalse-positive results at pH >7.0

Question 18

Quantification of urinary albumin

Answer 18

on a spot urine sample (ideally from a first morning void) bymeasurement of an albumin-to-creatinine ratio (ACR) is helpful in approximating a 24-h albumin excretion rate (AER), where ACR (mg/g) ≈AER (mg/24 h)

Tests to measure total
urine protein concentration accurately rely on precipitation with sulfosalicylic
or trichloracetic acid

Question 19

Traditionally, healthy individuals excrete

Answer 19

<150 mg/d of total protein and <30 mg/d of albumin.

Question 20

The glomerular basement membrane traps

most

Answer 20

large proteins (>100 kDa), and the foot processes of epithelial cells (podocytes) cover the urinary side of the glomerular basement membrane and produce a series of narrow channels (slit diaphragms)
to allow molecular passage of small solutes and water but not proteins

Question 21

EVALUATION OF PROTEINURIA

Answer 21

Microalbuminuria
30-300 mg/d or
30-300 mg/g

Macroalbuminuria
300-3500 mg/d or
300-3500 mg/g

Nephrotic range
> 3500 mg/d or
> 3500 mg/g

Question 22

Hypoalbuminemia in nephrotic syndrome occurs through

Answer 22

excessive urinary losses and increased proximal tubule catabolism of filtered albumin. Edema forms from renal sodium retention and reduced plasma oncotic pressure, which favors fluid movement from capillaries to interstitium

The urinary loss of regulatory proteins and changes in hepatic synthesis contribute to the other manifestations
of the nephrotic syndrome.

A hypercoagulable state may arise from urinary losses of antithrombin III, reduced serum levels of proteins
S and C, hyperfibrinogenemia, and enhanced platelet aggregation. Hypercholesterolemia may be severe and results from increased hepatic lipoprotein synthesis. Loss of immunoglobulins contributes to an increased risk of infection

Question 23

Hematuria is defined as

Answer 23

two to five RBCs per high-power field (HPF) and can be detected by
dipstick.
A false-positive dipstick for hematuria (where no RBCs are seen on urine microscopy) may occur when myoglobinuria is present, often in the setting of rhabdomyolysis.

Gross hematuria with blood clots usually is not an intrinsic renal process; rather, it suggests a postrenal source in the urinary collecting system

Question 24

Persistent or significant hematuria

Answer 24

(>3 RBCs/ HPF on three urinalyses, a single urinalysis with >100 RBCs, or gross hematuria) is associated with significant renal or urologic lesions in 9.1% of cases.

The level of suspicion for urogenital neoplasms in
patients with isolated painless hematuria and nondysmorphic RBCs increases with age.

Acute cystitis or urethritis in women can cause
gross hematuria. Hypercalciuria and hyperuricosuria are also risk factors for unexplained isolated hematuria in both children and adults. In some of these patients (50–60%), reducing calcium and uric acid excretion through dietary interventions can eliminate the microscopic hematuria

Question 25

Hematuria with
dysmorphic RBCs, RBC casts, and protein excretion >500 mg/d is
virtually diagnostic of

Answer 25

glomerulonephritis.

Question 26

WBC casts with bacteria are indicative of

Answer 26

pyelonephritis. WBCs and/or WBC casts also may be seen in acute glomerulonephritis as well as in tubulointerstitial processes such as interstitial nephritis and transplant rejection

Question 27

Casts can be seen in

Answer 27

chronic renal diseases. Degenerated cellular casts called waxy casts or broad casts (arising in the dilated tubules that have undergone compensatory hypertrophy in response to reduced renal mass) may be seen in the urine.

Question 28

true polyuria

Answer 28

(>3 L/d)

Polyuria results from two potential mechanisms:
(1) excretion of nonabsorbable solutes (such as glucose) or (2) excretion of water (usually from a defect in ADH production or renal responsiveness).

Question 29

The average person excretes between 600 and 800 mosmol of solutes per day, primarily
as urea and electrolytes.

Answer 29

If the urine output is >3 L/d and the
urine is dilute (<250 mosmol/L), total mosmol excretion is normal
and a water diuresis is present. This circumstance could arise from
polydipsia, inadequate secretion of vasopressin (central diabetes
insipidus), or failure of renal tubules to respond to vasopressin

Question 30

is due to subepithelial deposits, with resulting basement membrane reaction, resulting in the appearance of spike-like projections on silver stain

Answer 30

Membranous glomerulopathy

Question 31

There is mesangial expansion and endocapillary proliferation with cellular interposition in response to subendothelial deposits, resulting in the
“tram-track” of duplication of glomerular basement membrane

Answer 31

Membranoproliferative glomerulonephritis.

Question 32

Diabetic nephropathy. In the earliest stage of diabetic nephropathy, only mild mesangial increase and prominent glomerular
basement membranes (confirmed to be thickened by electron microscopy) are present (A). In slightly more advanced stages, more marked
mesangial expansion with early nodule formation develops, with evident arteriolar hyaline (B). In established diabetic nephropathy, there is
nodular mesangial expansion, so-called

Answer 32

Kimmelstiel-Wilson nodules

Question 33

Water is the most abundant constituent in the body, comprising approximately

Answer 33

50% of body weight in women and 60% in men.

Total body water is distributed in two major compartments: 55–75% is intracellular
(intracellular fluid [ICF]), and 25–45% is extracellular

The ECF is further subdivided into intravascular
(plasma water) and extravascular (interstitial) spaces in a ratio of 1:3.

Question 34

human body fluid osmolality

between

Answer 34

280 and 295 mOsm/kg.

AVP secretion is stimulated as systemic osmolality increases above a threshold level of ~285 mOsm/kg, above which there is a linear relationship
between osmolality and circulating AVP

Thirst and thus water ingestion are also activated at ~285 mOsm/kg, beyond which there is an equivalent linear increase in the perceived intensity of thirst as a function of circulating osmolality.

Question 35

AVP acts on renal, V2-type receptors in

Answer 35

the thick ascending limb of Henle and principal cells of the collecting duct (CD), increasing intracellular levels of cyclic AMP and activating protein kinase A (PKA)–dependent phosphorylation of multiple transport proteins

Question 36

aproximately

Answer 36

two-thirds of filtered Na+-Cl– is reabsorbed by the
renal proximal tubule, via both paracellular and transcellular

The TALH subsequently reabsorbs another 25–30% of filtered Na+-Cl– via the apical, furosemide- sensitive Na+-K+-2Cl– cotransporter.

Question 37

Approximately 9 L of fluid enter the gastrointestinal tract daily,

Answer 37

2 L by ingestion and 7 L by secretion; almost 98% of this volume is absorbed, such that daily fecal fluid loss is only 100–200 mL.

Question 38

Evaporation of water from the skin and respiratory tract (so-called
“insensible losses”) constitutes the major route for loss of solute-free
water, which is typically

Answer 38

500–650 mL/d in healthy adults.

Question 39

orthostatic tachycardia

Answer 39

(an increase of >15–20 beats/min upon standing), and
orthostatic hypotension (a >10–20 mmHg drop in blood pressure on standing).

Question 40

the urine Na+ concentration is typically

Answer 40

<20 mM in nonrenal causes of hypovolemia, with a urine osmolality of >450 mOsm/kg. The reduction in both GFR and distal tubular Na+ delivery may cause a defect in renal potassium excretion, with an increase in plasma K+ concentration.

hypovolemia and a hypochloremic alkalosis due to vomiting, diarrhea, or diuretics will typically have a urine Na+ concentration >20 mM and urine pH of >7.0, due to the increase in filtered HCO3 –;

the urine Cl– concentration in this setting is a more accurate indicator of volume status, with a level <25 mM suggestive of hypovolemia. The urine Na+ concentration is often >20 mM in patients with renal causes

Question 41

is the most appropriate resuscitation fluid for normonatremic or hyponatremic patients with severe hypovolemia; colloid solutions such as intravenous
albumin are not demonstrably superior for this purpose.
Hypernatremic patients should receive a hypotonic solution, 5% dextrose if there has only been water loss (as in diabetes insipidus), or hypotonic saline (1/2 or 1/4 normal saline) if there has been water and Na+-Cl– loss.

Answer 41

Isotonic, “normal” saline (0.9% NaCl, 154 mM Na+)

Patients with severe hemorrhage or anemia should receive red cell transfusions, without increasing the hematocrit beyond 35%.

Question 42

Hypovolemic Hyponatremia

Answer 42

UNa >20
Renal losses
Diuretic excess
Mineral corticoid deficiency
Salt-losing deficiency
Bicarbonaturia with
renal tubal acidosis and
metabolic alkalosis
Ketonuria
Osmotic diuresis
Cerebral salt wasting
syndrome

UNa <20
Extrarenal losses
Vomiting
Diarrhea
Third spacing of fluids
Burns
Pancreatitis
Trauma

Question 43

euvolemic

hyponatremia.

Answer 43

UNa >20

Glucocorticoid deficiency
Hypothyroidism
Stress
Drugs
Syndrome of inappropriate antidiuretic hormone secretion

Question 44

Thiazide diuretics cause hyponatremia via a number of mechanisms,

Answer 44

including polydipsia and diuretic-induced volume depletion.

Notably, thiazides do not inhibit the renal concentrating mechanism, such that circulating AVP retains a full effect on renal water retention.

In contrast, loop diuretics, which are less frequently associated with hyponatremia, inhibit Na+-Cl– and K+ absorption by the TALH, blunting the countercurrent mechanism and reducing the ability to concentrate the urine. Increased excretion of an osmotically active nonreabsorbable or poorly reabsorbable solute can also lead to volume depletion and hyponatremia;

important causes include glycosuria, ketonuria (e.g., in starvation or in diabetic or alcoholic ketoacidosis), and bicarbonaturia (e.g., in renal tubular acidosis or metabolic alkalosis, where the associated bicarbonaturia leads to loss of Na+).

Question 45

Hypervolemic Hyponatremia

Answer 45

UNa >20
Acute or chronic
renal failure

UNa <20
Nephrotic syndrome
Cirrhosis
Cardiac failure

Question 46

is the most frequent cause of euvolemic hyponatremia

Answer 46

The syndrome of inappropriate antidiuresis (SIAD)

Strictly speaking, patients with SIAD are not euvolemic but are subclinically volume-expanded, due to AVP-induced water and Na+-Cl– retention; “AVP escape” mechanisms invoked by sustained increases
in AVP serve to limit distal renal tubular transport, preserving a modestly hypervolemic steady state.

Serum uric acid is often low (<4 mg/dL) in patients with SIAD, consistent with suppressed proximal tubular transport in the setting of increased distal tubular Na+-Cl– and water transport; in contrast, patients with hypovolemic hyponatremia will often be hyperuricemic

Question 47

SIAD

also occurs with malignancies, most commonly with

Answer 47

Small-cell lung carcinoma (75% of malignancy associated SIAD); ~10% of patients with this tumor will have a plasma Na+ concentration of <130 mM at presentation

SIAD is also a frequent complication of certain drugs,
most commonly the selective serotonin reuptake inhibitors (SSRIs). Other drugs can potentiate the renal effect of AVP, without exerting direct effects on circulating AVP levels

Question 48

Hyponatremia can occasionally occur in patients with a very low intake of dietary solutes. Classically, this occurs in alcoholics whose sole nutrient is beer, hence the diagnostic label of

Answer 48

beer potomania; beer is very low in protein and salt content, containing only 1–2 mM of Na+

Question 49

The initial CNS response to acute

hyponatremia

Answer 49

is an increase in interstitial pressure, leading to shunting of ECF and solutes from the interstitial space into the cerebrospinal fluid and then on into the systemic circulation. This is

Question 50

Early symptoms hyponatremia can include

Answer 50

nausea, headache, and vomiting. However, severe complications can rapidly evolve, including seizure activity, brainstem herniation, coma, and death.

key complication of acute hyponatremia is normocapneic or hypercapneic respiratory failure; the associated hypoxia may amplify the neurologic injury. Normocapneic respiratory failure in this
setting is typically due to noncardiogenic, “neurogenic” pulmonary edema, with a normal pulmonary capillary wedge pressure.

Women, particularly before menopause, are much more likely than men to develop encephalopathy and severe neurologic sequelae.

Question 51

The recreational drugs
cause a rapid and potent induction of both thirst and AVP, leading to
severe acute hyponatremia

Answer 51

Molly and ecstasy, which share an
active ingredient (MDMA, 3,4-methylenedioxymethamphetamine),
cause a rapid and potent induction of both thirst and AVP, leading to
severe acute hyponatremia

Question 52

Persistent, chronic hyponatremia results in an efflux of organic osmolytes (creatine, betaine, glutamate, myoinositol, and taurine)
from brain cells; this response reduces intracellular osmolality and the
osmotic gradient favoring water entry.

Answer 52

This reduction in intracellular osmolytes is largely complete within 48 h, the time period that clinically
defines chronic hyponatremia

chronic hyponatremia does not fully protect patients
from symptoms, which can include vomiting, nausea, confusion, and
seizures, usually at plasma Na+ concentration <125 mM

Question 53

Rapid correction of hyponatremia (>8–10

mM in 24 h or 18 mM in 48 h)

Answer 53

is also associated with a disruption in integrity of the blood-brain barrier, allowing the entry of immune
mediators that may contribute to demyelination.

Question 54

The lesions of ODS classically affect the

Answer 54

pons, a structure wherein the delay in the reaccumulation of osmotic osmolytes is particularly pronounced;

clinically, patients with central pontine myelinolysis can present 1 or more days after overcorrection of hyponatremia with paraparesis or quadriparesis,
dysphagia, dysarthria, diplopia, a “locked-in syndrome,” and loss of consciousness.

Question 55

in order of frequency, the lesions of extrapontine

myelinolysis can occur in the cerebellum, lateral geniculate body, thalamus, putamen, and cerebral cortex or subcortex

Answer 55

Clinical presentation of ODS can, therefore, vary as a function of the extent and localization of extrapontine myelinolysis, with the reported development of

ataxia, mutism, parkinsonism, dystonia, and catatonia.
Relowering of plasma Na+ concentration after overly rapid correction can prevent or attenuate ODS

Question 56

Serum glucose should also be measured; plasma Na+ concentration falls by

Answer 56

~1.6–2.4 mM for every 100-mg/dL increase in glucose,

Question 57

the ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia

Answer 57

is the demonstration that plasma Na+ concentration corrects after hydration with normal saline.

Question 58

A urine osmolality <100 mOsm/kg

Answer 58

is suggestive of polydipsia; urine osmolality >400 mOsm/kg indicates that AVP excess is playing a more dominant role

Question 59

Patients with hyponatremia

due to decreased solute intake

Answer 59

(beer potomania) typically have urine
Na+ concentration <20 mM and urine osmolality in the range of <100 to the low 200s. Finally, the measurement of urine K+ concentration
is required to calculate the urine-to-plasma electrolyte ratio, which is useful to predict the response to fluid restriction

Question 60

patients with chronic hyponatremia, present for

Answer 60

> 48 h, are less likely to have severe symptoms. Second, patients with chronic hyponatremia are at risk for ODS if plasma Na+ concentration is corrected
by >8–10 mM within the first 24 h and/or by >18 mM within the first 48 h.

Question 61

Insensible Losses

Answer 61

~10 mL/kg per day: less if ventilated, more if febrile

Question 62

Many patients with SIAD respond to combined therapy with

Answer 62

oral furosemide, 20 mg twice a day (higher doses may be necessary in renal insufficiency), and oral salt tablets;

furosemide serves to inhibit the renal countercurrent mechanism and blunt urinary concentrating ability, whereas the salt tablets counteract diuretic-associated natriuresis.

Question 63

is a potent inhibitor of principal cells and can
be used in patients whose Na levels do not increase in response to furosemide and salt tablets.

However, this agent can be associated with a reduction in GFR, due to excessive natriuresis and/or direct renal toxicity; it should be avoided in cirrhotic patients in particular, who are at higher risk of nephrotoxicity due to drug accumulation.

Answer 63

Demeclocycline

Question 64

are highly effective in SIAD and in hypervolemic hyponatremia due to heart failure or cirrhosis, reliably increasing plasma Na+ concentration due to their “aquaretic” effects (augmentation of free water clearance).

Answer 64

AVP antagonists (vaptans)

Most of these agents specifically antagonize the V2 AVP receptor; tolvaptan is currently the only oral V2 antagonist to be approved by the U.S. Food and Drug

Question 65

the only available intravenous vaptan,
is a mixed V1A/V2 antagonist, with a modest risk of hypotension due
to V1A receptor inhibition. Therapy with vaptans must be initiated in
a hospital setting, with a liberalization of fluid restriction (>2 L/d) and

Answer 65

Conivaptan

Abnormalities in liver function tests
have been reported with chronic tolvaptan therapy; hence, the use of this agent should be restricted to <1–2 months.

Question 66

Treatment of acute symptomatic hyponatremia should include

Answer 66

hypertonic 3% saline (513 mM) to acutely increase plasma Na+ concentration by 1–2 mM/h to a total of 4–6 mM; this modest increase is typically sufficient to alleviate severe acute symptoms

The administration of supplemental oxygen
and ventilatory support is also critical in acute hyponatremia, in the event that patients develop acute pulmonary edema or hypercapneic
respiratory failure

AVP antagonists do not have an approved role in the management of acute hyponatremia.

Question 67

hyponatremia can be safely reinduced or

stabilized by the administration of the AVP agonist

Answer 67

desmopressin acetate (DDAVP) and/or the administration of free water, typically
intravenous D5W; the goal is to prevent or reverse the development of ODS

Alternatively, the treatment of patients with marked hyponatremia can be initiated with the twice-daily administration of DDAVP to maintain constant AVP bioactivity, combined with the administration
of hypertonic saline to slowly correct the serum sodium in a more controlled fashion, thus reducing upfront the risk of overcorrection

Question 68

is, in turn, the most common gastrointestinal

cause of hypernatremia.

Answer 68

Diarrhea

Notably, osmotic diarrhea and viral gastroenteritides
typically generate stools with Na+ and K+ <100 mM, thus leadingto water loss and hypernatremia;

Question 69

is characterized by renal resistance to AVP, which can be partial or complete

Answer 69

Nephrogenic DI (NDI)

Question 70

can also cause polyuria and NDI; calcium signals directly through the calcium-sensing receptor to downregulate Na+, K+, and Cl– transport
by the TALH and water transport in principal cells,

Answer 70

hypercalcemia.

thus reducing renal concentrating ability in hypercalcemia

Lithium causes NDI by multiple mechanisms, including
direct inhibition of renal glycogen synthase kinase-3 (GSK3), a kinase thought to be the pharmacologic target of lithium in bipolar disease; GSK3 is required for the response of principal cells to AVP.

Question 71

As in hyponatremia, the symptoms of hypernatremia are predominantly neurologic.

Answer 71

Altered mental status is the most frequent manifestation, ranging from mild
confusion and lethargy to deep coma.

The sudden shrinkage of brain cells in acute hypernatremia may lead to parenchymal or subarachnoid hemorrhages and/or subdural hematomas; however, these vascular complications are primarily encountered in pediatric and neonatal
patients

Question 72

Many patients with hypernatremia are

Answer 72

polyuric; should an osmotic diuresis be responsible, with excessive excretion of Na+-Cl–, glucose,
and/or urea, then daily solute excretion will be >750–1000 mOsm/d (>15 mOsm/kg body water per day

Question 73

a water deprivation test is unnecessary in hypernatremia; indeed, water deprivation is absolutely contraindicated in this setting,

Answer 73

given the risk for worsening the hypernatremia.

Patients with NDI will fail to respond to DDAVP, with a urine osmolality that increases by <50% or <150 mOsm/kg from baseline, in combination with a normal
or high circulating AVP level; patients with central DI will respond to DDAVP, with a reduced circulating AVP. Patients may exhibit a partial response to DDAVP, with a >50% rise in urine osmolality that nonetheless fails to reach 800 mOsm/kg; the level of circulating AVP will help differentiate the underlying cause

Patients with central DI should respond to the administration of intravenous, intranasal, or oral DDAVP. Patients with NDI due to lithium may
reduce their polyuria with amiloride (2.5–10 mg/d), which decreases entry of lithium into principal cells by inhibiting ENaC

Question 74

may reduce polyuria due to NDI, ostensibly

by inducing hypovolemia and increasing proximal tubular water reabsorption.

Answer 74

Thiazides

Question 75

have been used to treat polyuria associated with NDI,

reducing the negative effect of intrarenal prostaglandins on urinary concentrating mechanisms;

Answer 75

Occasionally, nonsteroidal anti-inflammatory drugs
(NSAIDs)

however, this assumes the risks of
NSAID-associated gastric and/or renal toxicity