1
Q
cellular response to chronic hyponatremia does not fully protect patients from symptoms, which can include vomiting, nausea, confusion, and seizures, usually at plasma Na+ concentration
A
<125 mM
2
Q
What is the expected urine findings in SIAD
A
Urine Na >20
Hypouricemia <4mg/dl
3
Q
What is the ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia
A
demonstration that plasma Na+ concentration corrects after hydration with normal saline
4
Q
What is the formula for Na deficit and goal correction for Acute vs Chronic Hyponatremia
A
Na+ deficit = 0.6 x body weight x (target plasma Na+ concentration – starting plasma Na+ concentration)
Acute 4-6 mM
Chronic 6-8 mM
5
Q
Polydipsia
Hypertonic saline infusion then measure copeptin (indirect water deprivation test)
Increases level of copeptin?
A
Polydipsia rather than central DI
6
Q
Response to desmopressin
Central DI
Nephrogenic Di
A
Central DI
Reduced AVP and copeptin
Increases level urine osm
Nephrogenic DI
High levels AVP and copeptin
Low urine osm (<50% increase or <150 mOsm/kg from baseline)
7
Q
In the event that the plasma Na+ concentration overcorrects following therapy, be it with hypertonic saline, isotonic saline, or a vaptan, hyponatremia can be safely reinduced or stabilized by the administration of
A
Desmopressin (AVP agonist)
8
Q
Electrocardiographic changes in hypokalemia
A
broad flat T waves, ST depression, and QT prolongation; these are most marked when serum K+ is <2.7 mmol
9
Q
ECG manifestations in hyperkalemia progress
5.5-6.5 mM
6.5-7.5 mM
7.0-8.0 mM
>8.0 mM
A
5.5-6.5 mM: tall peaked T
6.5-7.5 mM: loss of P
7.0-8.0 mM: wide QRS
>8.0 mM: sine wave
10
Q
first step in the diagnostic evaluation of hyper- or hypocalcemia is to
A
ensure that the alteration in serum calcium levels is not due to abnormal albumin concentrations
**corrected calcium
adding 0.2 mM (0.8 mg/dL) to the total calcium level for every decrement in serum albumin of 1.0 g/ dL below the reference value of 4.1 g/dL for albumin, and, conversely, for elevations in serum albumin
11
Q
PTH level is increased (or “inappropriately normal”) in the setting of elevated Ca and low phosphorus
What is the dx?
A
Primary hyperthyroidism
*vs FHH (low CaCr ratio)
CaCr ratio <0.01
12
Q
Initial therapy of significant hypercalcemia begins with volume expansion because hypercalcemia invariably leads to dehydration; how many liters in the first 24h?
A
4–6 L of intravenous saline may be required over the first 24 h
13
Q
In patients with 1,25(OH)2D-mediated hypercalcemia, what is the preferred therapy
A
glucocorticoids
Intravenous hydrocortisone (100–300 mg daily) or oral prednisone (40–60 mg daily) for 3–7 days
14
Q
is a cardinal feature of autoimmune endocrinopathies
A
Hypoparathyroidism
15
Q
Nutritional vitamin D deficiency is best assessed by obtaining
A
serum 25-hydroxyvitamin D levels
- In the setting of renal insufficiency or suspected vitamin D resistance, serum 1,25(OH)2D levels are informative
16
Q
an elevated PTH level (secondary hyperparathyroidism) should direct attention to what cause of hypocalcemia?
A
Vitamin D axis
17
Q
Urine chemistry for pre renal AKI
A
Low FENa ≤1%, U/P Cr ≥40, UNa ≤10, U/P Osm ≥1
- Concentrated acid urine, hyaline casts,
crystalluria
18
Q
Urine chemistry for renal AKI
A
FENa 1–3%, U/P Cr ≤40, UOsm ~Isomotic
- “Muddy brown” granular casts, hematuria, dysmorphic RBCs, RBC casts in GN, WBC casts in AIN, eosinophils in atheroemboli
19
Q
Postinfectious GN is to be distinguished from synpharyngitic hematuria.
What are their differences
A
Synpharyngitic hematuria, usually with a viral pharyngitis, is most often related to IgA nephropathy rather than postinfectious GN
Demonstrates normal circulating C3 compared to low C3 in PIGN
20
Q
Recent exposure (up to 2 weeks) to NSAIDs, ampicillin, PPI, sufa drugs presenting with rapid loss of kidney fx and fever, rash, and eosinophilia
What is the dx?
A
Allergic interstitial nephritis (AIN)
Eosinophilia atypical for nsaids
21
Q
What is the most characteristic cell types in AIN?
A
activated T lymphocytes and plasma cells, along with some white blood cell casts
22
Q
Non inflammatory interstitial diseases
Name the exposure
A) Fanconi syndrome
B) hypoMg + AKI
C) Nephrogenic DI
D) hypoK + intersitial dse
A
A) Fanconi- ifosfamide, heavy metals
B) hypoMg + AKI- platinum based chemo
C) nephrogenic DI- lithium, analgesics, chemo
D) hypoK +interstitial dse- aminoglycosides (+ hearing loss) or amphotericin B (+ RTA)
23
Q
When a patient with inflammatory bowel disease or one who has had gastric bypass procedures such as the Roux-en-Y develops kidney injury, with or without calcium oxalate kidney stones, what should be done?
A
a 24-h urine oxalate measurement must be determined to diagnose intestinal hyperoxaluria
24
Q
What conditions cause papillry necrosis associated with chronic interstitial damage characterized by nephrogenic diabetes insipidus?
A
PADS- papillary necrosis, analgesics, DM, sickle cell
DM, chronic analgesic use, or sickle-cell diseases
25
3 defining features in Nephrotic syndrome
Edema
Hypoalbuminemia (<3.5g/dl)
Proteinuria (>3.5g/d)
*high LDL, low HDL and lipiduria
26
characteristic finding of rapid-onset hypoalbuminemia in NS is horizontal linear white lines in the nail bed
Muehrcke’s lines
27
Bartters’s syndrome vs Gitelman’s syndrome
Bartters
-abnormal loop of henle fx
-hypokalemic alkalosis
-Hypercalciuria
-inability to concentrate urine
Gitelmans
-defect in thiazide-sensitive NaCl transporter
-hypochloremic hypokalemic met alkalosis
-hypocalciuria
-preserved ability to concentrate urine
28
Renal blood flow accounts for how many % of the CO?
20%
29
Renal autoregulation fails once SBP falls below
80mmHg
30
Type of HRS in which AKI persists despite volume administration and withholding of diuretics
Type 1 poor prognosis
31
Type of HRS that is a less severe form characterized mainly by refractory ascites
Type 2
32
abdominal compartment syndrome, where markedly elevated intraabdominal pressures, usually ____ mmhg, lead to renal vein compression and reduced GFR
>20 mmHg
33
Gadolinium (group 1) has been associated with development of
nephrogenic systemic fibrosis (NSF)
* The risk of AKI associated with standard doses of group II gadolinium-based contrast media is very low
34
What agent causes non oliguric AKI and tubular necrosis with hypomagnesemia after 5-7 days of therapy and can present even after the drug has been discontinued?
Aminoglycosides
35
Agent that binds to tubular membrane cholesterol and introduces pores. Clinical features of nephrotoxicity include polyuria, hypomagnesemia, hypocalcemia, and nongap metabolic acidosis
amphotericin B
36
Agent that can precipitate in tubules and cause AKI by tubular obstruction, particularly when given as an intravenous bolus at high doses (500 mg/m2) or in the setting of hypovolemia
Acyclovir
37
What chemotherapeutic agent cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi syndrome), polyuria, hypokalemia, and a modest decline in GFR?
Ifosfamide
38
antineoplastic agents that may cause thrombotic microangiopathy with resultant AKI
mitomycin C and gemcitabine
39
What is thought to be responsible for tubular injury in diethylene glycol toxicity?
2-hydroxyethoxyacetic acid (HEAA)
40
found to be the cause of “Chinese herb nephropathy” and “Balkan nephropathy
Aristolochic acid
Anemia may be disproportionately severe relative to level of kidney function
41
AKI is currently defined by
rise from baseline of at least 0.3 mg/dL within 48 h or at least 50% higher than baseline within 1 week, or a reduction in urine output to <0.5 mL/kg per h for longer than 6 h
42
The most common clinical course of contrast nephropathy
a rise in SCr beginning 24–48 h following exposure, peaking within 3–5 days, and resolving within 1 week
43
Lab test suggestive of CKD
Normocytic anemia w/o blood loss
Secondary hyperparathyroidism with hyperPhosphatemia and hypoCalcemia
44
FeNa typically >1%
Give etiology
Ischemia associated AKI
Tubular injury- Aminoglycoside antibiotics, cisplatin, tenofovir, vancoycin, zoledronate, ethylene glycol, aristolochic acid, and melamine
45
Noted with recent manipulation of aorta or large vessels presenting with retinal plaques, palpable purpura, livedo reticularis. Lab features of hypocomplementemia, eosinophiluria and variable amounts of protein
Atheroembolic disease
46
Presents with Renal tubular epithelial (RTE) cells, RTE casts, Pigmented casts?
A. Pyelonephritis?
B. TTP?
C. Allergic interstitial nephritis?
D. Acute cellular autograft rejection
D. Acute cellular autograft rejection
47
The finding of oxalate crystals in AKI should prompt an evaluation for what toxicity?
Ethylene glycol
48
AKI often leads to
K?
P?
Ca?
hyperkalemia, hyperphosphatemia, and hypocalcemia
HyperP + HYPOca= rhabdo or TLS
Rhabdo: high CK and urea
TLS: normal CK and markedly high uric acid
49
In cases of oliguric AKI, the urinary flow rate in response to bolus intravenous furosemide 1.0–1.5 mg/kg can be used a prognostic test. What would indicate a higher risk of progression to more severe AKI?
UO <200ml over 2h after IV furosemide
50
What is the definitive treatment of the hepatorenal syndrome
Orthotopic liver transplantation
51
Protein intake in AKI
0.8–1.0 g/kg per day in noncatabolic AKI without the need for dialysis;
1.0–1.5 g/kg per day in patients on dialysis;
maximum of 1.7 g/kg per day if hypercatabolic and receiving continuous renal replacement therapy
52
Measurement of this after an AKI episode can help predict the risk of kidney disease progression and can serve as a valuable riskstratification tool
albuminuria
53
UACR thresholds as a marker not only for early detection of primary kidney disease but for systemic microvascular disease as well
UACR >2.5 mg/mmol (male) or >3.5 mg/mmol (female) on two to three occasions
54
Clinical manifestations of severe hyperparathyroidism include
bone pain and fragility, brown tumors, compression syndromes, and resistance to erythropoiesis-stimulating agents (ESA)
55
characterized by reduced bone volume and mineralization and may result from excessive suppression of PTH production, chronic inflammation, or both characterized by reduced bone volume and mineralization and may result from excessive suppression of PTH production, chronic inflammation, or both
Adynamic bone disease
56
Complications of adynamic bone disease include an increased incidence of fracture and bone pain and an association with increased vascular and cardiac calcification. Occasionally, the calcium will precipitate in the soft tissues into large concretions termed
Tumoral calcinosis
57
a distinct process, consequent to reduced production and action of 1,25(OH)2D3, leading to
Osteomalacia
58
In CKD, It is heralded by painful livedo reticularis and subcutaneous nodules that advance to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts
Calciphylaxis
* warfarin treatment is considered a risk factor for calciphylaxis
59
enhance the sensitivity of parathyroid cells to the suppressive effect of calcium. This produces a dose-dependent reduction in PTH and plasma calcium concentration in some patients
Calcimimetic agents: cinacalcet and etelcalcetide
* target PTH level between 2 and 9 times the upper limit of normal
60
is the leading cause of morbidity and mortality in patients at every stage of CKD
Cardiovascular disease
61
Which is not a traditional risk factor in the development of vascular disease in CKD?
A. DM
B. OSA
C. Hyperhomocysteinemia
D. Sympathetic overactivity
B. OSA
Traditional risk factors include hypertension, diabetes mellitus, hypervolemia, dyslipidemia, sympathetic overactivity, and hyperhomocysteinemia
62
Which of the following is a. CKD related risk in development of vascular dse?
A. Dyslipidemia
B. Hypervolemia
C. Hypertension
D. Systemic inflammation
D. Systemic inflammation
The CKD-related risk factors comprise anemia, hyperphosphatemia, hyperparathyroidism, increased FGF-23, sleep apnea, and systemic inflammation
63
are the principal causes of sudden cardiac death in dialysis patients
Asystole and bradyarrhythmias
64
What are the most common complications of CKD?
Hypertension and LVH
65
What is “reverse causation” in dialysis patients?
low blood pressure actually carries a worse prognosis than does high blood
presence of traditional risk factors, such as hypertension, hyperlipidemia, and obesity, appear to portend a better prognosis
66
CKD patient with DM or proteinuria >1g/day has BP of 140/90. You target to reduce BP to <130/80. What is the first line of therapy?
A. ACEi
B. ARBs
C. Salt restriction
D. Water restriction
C. Salt restriction
Salt restriction should be the first line of therapy
67
Current practice is to target a hemoglobin concentration of ___ in CKD
Hgb 100-115 g/L
68
Which stage if CKD?
A. Anemia
B. Uremic neuromuscular dse
C. Peripheral neuropathy
D. Educational programs should be commenced
E. Should minimize exposure to gadolinium
A. Stage 3, universal by Stage 4
B. Stage 3
C. Stage 4
D. No later than stage 4
E. Stage 3, avoid in Stage 4-5
69
Commonly accepted criteria for initiating patients on maintenance
AEIOU
Acidosis, electrolytes (hyperK), increased bleeding, overload, uremic sx, eGFR <10
70
What is the most common acute complication of hemodialysis, particularly among which patients.
Hypotension
Among patients with DM
71
Management if hypotension during dislysis
- D/C ultrafiltration, bolus of 100-250ml isotonic saline
- avoid excessively rapid fluid removal (>13 ml/kg/h)
- ultrafiltration modeling (more fluid is removed at the beginning)
- sequential ultrafiltration followed by dialysis, cooling of dialysis
- avoid heavy meals during dialysis
*insufficient evidence for Midodrine
72
attributed to an IgEmediated intermediate hypersensitivity reaction to ethylene oxide used in the sterilization of new dialyzers. This reaction typically occurs soon after the initiation of a treatment (within the first few minutes) and can progress to full-blown anaphylaxis
Type A reactions
Tx: steroids or epinephrine
73
consists of a symptom complex of nonspecific chest and back pain, which appears to result from complement activation and cytokine release. These symptoms typically occur several minutes into the dialysis run and typically resolve over time with continued dialysis
Type B reaction
74
What are the absolute contraindications to kidney transplantation
chronic illness that limits predicted survival for <2 years, active malignancy, active infection, psychosocial issues affecting adherence to the medical care, and active substance abuse
75
De novo diabetes mellitus following transplantation more commonly occurs with?
Tacrolimus
76
The most common malignant lesions in patients on immunosuppressive therapy
Cancer of the skin and lips
77
The most common late (>6 mos) opportunistic infection in renal transplant recipients
BAN 3H
BK virus
Aspergillus
Nocardia
Herpes zoster, hep B, hep C
78
Urologic intervention should be postponed unless there is
evidence of UTI,
a low probability of spontaneous stone passage (e.g., a stone measuring >6 mm or an anatomic abnormality), or
intractable pain
79
Calcium oxalate stone treatment
Avoidance of Vitamin C
Thiazide (Chlorthalidone)
Na restriction <2.5g/d
Allopurinol?
Urine pH does not matter
79
Calcium phosphate stone tx
Thiazide (Chlorthalidone)
Na restriction <2.5g/d
Alkali supplements (K citrate or bicarbonate)
80
Uric acid stone tx
Mainstay is increase urine pH
K based bicarb or citrate
Allopurinol/ Febuxostat
81
Cystine stone tx
Tiopronin (preferred) or penicillamine
K citrate/ bicarb
82
Struvite stone infection with urease-producing bacteria
Proteus mirabilis
Klebsiella pneumoniae
Providencia
83
associated with the production of gas in renal and perinephric tissues and occurs almost exclusively in diabetic patients
Emphysematous pyelonephritis
84
occurs when chronic urinary obstruction (often by staghorn calculi), together with chronic infection, leads to suppurative destruction of renal tissue. On pathologic examination, the residual renal tissue frequently has a yellow coloration, with infiltration by lipid-laden macrophages
Xanthogranulomatous pyelonephritis
85
renal failure in glomerulonephritis best correlates histologically with the appearance of?
tubulointerstitial nephritis
86
Guve the values
Normal urine albumin
Microalbuminuria
Frank proteinuria
Sustained proteinuria
Benign/ functional / transient proteinuria
N: 8-10mg/d
Micro: 30-300 mg/d
Frank: >300 mg/d
Sustained: 1-2 g/d
Benign: <1 g/d
87
Proteinuria in adults
Vs children
Non selective while in children it is selective
Proteinuria in most adults with glomerular disease is nonselective, containing albumin and a mixture of other serum proteins, whereas in children with minimal change disease (MCD), the proteinuria is selective and composed largely of albumin
88
the most common causes of glomerulonephritis throughout the world
Malaria and schistosomiasis
Followed by HIV, hep B and C
89
Poststreptococcal glomerulonephritis due to pharyngitis develops how many weeks after infection?
after impetigo?
1–3 weeks pharyngitis
2–6 weeks impetigo
90
renal biopsy showed hypercellularity of mesangial and endothelial cells; glomerular infiltrates of polymorphonuclear leukocytes; granular subendothelial immune deposits of IgG, IgM, C3, C4, and C5–9; and subepithelial deposits (which appear as “humps”). What will confirm the dx?
Post streptococcal glomerulonephritis
Positive cultures for streptococcal infection are inconsistently present (10–70%), but increased titers of ASO (30%), anti-DNAse (70%), or antihyaluronidase antibodies (40%) can help confirm the diagnosis
*rarely requires biopsy
91
True or false
In PSGN, There is no role for immunosuppressive therapy, even in the setting of crescents
True
92
kidneys have subcapsular hemorrhages with a “flea-bitten” appearance, and microscopy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial immune deposits of IgG, IgM, and C3
Tx?
Endocarditis-associated glomerulonephritis
4-6 weeks of antibiotics
*usually in culture negative SBE or right sided endocarditis
93
on biopsy by linear immunofluorescent staining for IgG (rarely IgA). Positive for antibodies to a3 NC1 domain of collagen IV
What is the tx?
Goodpasture syndrome
8–10 treatments of plasmapheresis accompanied by oral prednisone and cyclophosphamide
94
ANCA small vessel vasculitis
*pauci-immune glomerulonephritis*
Positive anti-PR3
Positive anti-MPO
Anti-PR3: granulomatous polyangiitis
Anti-MPO: Churg-strauss or microscopic polyangiitis
95
Px with fever, purulent rhinorrhea, nasal ulcers, sinus pain, polyarthralgias/arthritis, cough, hemoptysis, shortness of breath, hematuria, and subnephrotic proteinuria
Chest x-ray often reveals nodules and persistent infiltrates, sometimes with cavities
Renal biopsies during active disease demonstrate segmental necrotizing glomerulonephritis without immune deposits
Granulomatosis with polyangiitis
96
on renal biopsy shows no glomerular lesion by light microscopy and is negative for deposits by immunofluorescent microscopy or occasionally shows small amounts of IgM in the mesangium. Electron microscopy, however, consistently demonstrates an effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes
Minimal Change disease
97
Adults with MCD are considered steroid resistant if they fail to respond after how many months?
4 months of therapy
*may have FSGS on repeat biopsy
98
Although thrombotic complications are a feature of all nephrotic syndromes, which has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep vein thrombosis
MGN
99
Adults with MCD are considered steroid resistant if they fail to respond after how many months?
4 months of therapy
*may have FSGS on repeat biopsy
100
When do morphologic changes appear in the kidney in diabetic nephropathy?
Within 1-2 years
101
Testing for microalbuminuria in DM
Type 1?
Type 2?
5 yrs after diagnosis and yearly thereafter
At tie of diagnosis and yearly thereafter
102
develop hematuria, thinning and splitting of the GBMs, and mild proteinuria and renal failure in association with sensorineural deafness. Some patients develop lenticonus of the anterior lens capsule, “dot and fleck” retinopathy, and rarely, leiomyomatosis. What is the mutation?
Alport syndrome
A5(IV) Collagen chain
103
Criteria for ADPKD
15-29 yo
30-59 yo
60 above
at least two renal cysts (unilateral or bilateral
at least two cysts in each kidney
at least four cysts in each kidney
104
UA crystal findings
A) Sulfadiazine for toxoplasmosis
B) indinavir for HIV
C) Acyclovir for herpes
A) sheaf of wheat for sulfonamide crystals
B) individual or parallel clusters of needle shaped indinavir
C) red-green birefringent needle shaped crystals of acyclovir
105
after prolonged exposure, produces renal interstitial fibrosis with a relative paucity of cellular infiltrates. The urine sediment is bland, with rare leukocytes and only mild proteinuria. Anemia may be disproportionately severe relative to the level of kidney dysfunction
Aristolochic acid nephropathy
106
Which type of stones are most commonly seen in patients with ADPKD?
a. Calcium oxalate
b. Calcium phosphate
c. Struvite
d. Uric acid
D. Uric acid
Source: HPIM 21st ed. Ch 315 p2351
Kidney stones occur in ~20% of patients with ADPKD
Different from the general population, more than half of the stones in patients with ADPKD are composed of uric acid, with the remainder due to calcium oxalate
107
Which characteristic correctly describes a cortical nephron?
A. Possesses a long loop of Henle
B. Associated with vasa recta
C. Has a larger afferent than efferent arteriole
D. Maintains the interstitial osmotic gradient
C. Has a larger afferent than efferent arteriole
108
Which is correctly arranged from largest to smallest sodium reabsorption contribution?
A. Loop of Henle > Collecting Duct > Proximal Tubule
B. Loop of Henle > Proximal Tubule > Distal Convoluted Tubule
C. Proximal Tubule > Distal Convoluted Tubule > Loop of Henle
D. Proximal Tubule > Loop of Henle > Collecting Duct
D. Proximal Tubule > Loop of Henle > Collecting Duct
The relative contributions of the different nephron segments in sodium reabsorption are summarized as follows:
Proximal Tubule: 60%
Loop of Henle: 15 - 25% (mainly thick ascending limb)
Distal Convoluted Tubule: 5%
Collecting Duct: 4 - 5%
109
Phenomenon where spontaneous urinary sodium excretion and diuresis occur after a period of initial sodium retention from volume expansion?
Aldosterone escape
110
Which is NOT an expected long-term complication after recovery from acute kidney injury?
A. Accelerated chronic kidney disease
B. Death
C. Increased infection risk
D. Renal replacement therapy
C. Increased infection risk
Outcome and prognosis of AKI
- higher mortality
- longer length of stay
- progression of CKD
- increased risk of later cardiovascular events
** Measurement of albuminuria after an AKI episode can help predict the risk of kidney disease progression and can serve as a valuable riskstratification tool
111
Drugs that elevate creatinine levels without actual change in eGFR
CreaTinine= Cimetidine and Trimethoprim
112
How often should patients with risk factors for CKD but normal GFR be monitored for development of renal abnormalities?
Every 2 years
113
Targets for adequacy for determining dialysis adequacy
A) urea reduction ratio
B) Kt/V
A) urea reduction ratio of > 65-70%
B) Kt/V > 1.2 or 1.05
114
Which chronic electrolyte/metabolic abnormality is associated with a tubular lesion characterized by vacuolar degeneration of the proximal and distal tubular cells?
A. Hypophosphatemia
в. Hypokalemia
c. Hypocalcemia
D. Hypercalcemia
B. Hypokalemia
115
Match the nephropathy with corresponding tubulointerstitial lesion
A. Focal degenerative change in renal epithelia, primarily in collecting ducts, distal tubules and loops of henle
B. Vacuolar degeneration of proximal and distal tubular cells
C. Renal interstitial fibrosis with relative paucity of cellular infiltrates
D. Patchy interstitial fibrosis and tubular atrophy, often in striped pattern
E. Triad of saturnine gout, hypertension and impaired kidney function
A. Hypercalcemic nephropathy
B. Hypokalemic nephropathy
C. Aristocholic acid nephropathy
D. CNI nephropathy
E. Lead nephropathy
116
A 51/M, known hypertensive, was referred due to the following laboratory findings: serum sodium 138 meq/L, potassium 3.1 meq/L; urine studies show a pH of 6.0. KUB USG showed nephrolithiasis.
Which among the following conditions is the most likely diagnosis?
A. Type I renal tubular acidosis
B. Proximal renal tubular acidosis
С. Type Ill renal tubular acidosis
D. Generalized distal renal tubular acidosis
A. Type 1
117
A 48/F presented to the clinic with palpitation and a five-year history of low potassium level and hypertension. She was initially treated with potassium supplements. Her cardiac work-up including echocardiography, stress test and Holter monitoring were all negative. After 2 months, she was admitted to the hospital with an acute hypertensive episode and hypokalemia.
On evaluation, she was found to have low aldosterone levels. Cortisol level is normal.
Urine potassium and transtubular potassium gradient are both elevated.
What is the most likely diagnosis?
A. Cushing's Syndrome
B. Malignant hypertension
C. Renin-secreting tumor
D. Liddle's Syndrome
D. Liddle's Syndrome
118
etiologies of CKD that may cause disproportionate hyperkalemia with decline in GFR?
Diabetes
Obstructive uropathy
Sickle cell nephropathy
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