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Nephrology > Deck 1 > Flashcards

Deck 1 Flashcards

1
Q

AVF is too deep for needling - what should you do?

A

Button Hole Technique.

Track is created with repetitive cannulation of the same path by sharp needles, followed by blunt needle cannulation.

  • Downside is associated with higher rate of infections.
  • You cannot use buttonhole with AV graft
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2
Q

First line antibiotic for MSSA Bacteraemia in dialysis patient

A

IV Cefazolin after dialysis

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3
Q

Best option for obese patient trying to get listed for kidney transplant?

A

Bariatric Surgery

Recent data show that sleeve gastrectomy has become the most commonly performed bariatric surgery in patients with ESRD.

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4
Q

AKI in intubated patient with decompensated cirrhosis.

Best treatment for hyperammonemia (setting of cirrhosis) and acute cerebral oedema?

A

Intermittent Dialysis

Ammonia levels of greater than 200 have been correlated with increased intracranial pressure and brain herniation. AKI worsens hyperammonemia as the kidneys normally excrete 20% of the daily ammonia load
Ammonia has a molecular mass of 17g/mol - no significant protein binding so can be removed effectively by intermittent HD - which can improve survival inpatients with cerebral oedema. Danger of rebound often necessitates initiation of CVVHDF

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5
Q

Medical treatment of hyperammonemia

A

Restriction of protein intake, correction of hypoglycaemia, correction of any fluid or electrolye imbalance + lactulose and rifaximin.

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6
Q

What effect does cerebral salt wasting have on urinary studies?

A

High urinary sodium

High urinary chloride

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7
Q

What effect does diuretic abuse have on urinary studies?

A

High urinary sodium

High urinary chloride

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8
Q

AKI/ CKD/ Nephrotic Syndrome - kidney biopsy electron microscopy demonstrates organised fibrillar deposits > 30nm in diameter arranged in parralel arrays of microtubular structures

A

Immunotactoid GN.

May be idiopathic
May be associated with underlying autoimmune conditions, plasma cell dyscrasias or malignancy

Progression to ESRD is not uncommon.

Case reports describe the use of rituximab, corticosteroids, cyclophosphamide and MMF to treat immunotactoid GN but never initiate treatment without prior investigation for a cause.

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9
Q

What size are amyloidosis fibrils on EM?

A

10-nm fibrils= Amyloidosis

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10
Q

What size are fibrillary GN fibrils on EM?

A

20-nm fibrils= Fibrillary GN

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11
Q

What size are fibrils associated with cryoglobulinaemic GN and what is their associated pattern?

A

40-nm fibrils = Cryoglobulinaemic GN

Frequently have a fingerprint pattern.

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12
Q

What is the appropriate regimen to prevent graft failure in a patient with a history of thrombosis?

A

Dipyridamole and Aspirin

A prospective, randomized, double-blind, parallel group trial examined the efficacy of dipyridamole and/or aspirin in decreasing the rate of thrombosis in polytetrafluoroethylene grafts. Neither drug therapy improved patency in patients with previous thrombosis of an existing graft, but thrombosis rates were significantly reduced in new AV grafts in patients who had received dipyridamole.

No benefit to aspirin + clopidogrel or warfarin

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13
Q 
30 year old woman has recurrent nephrolithiasis. She appears well + normotensive. CT scan demonstrates nephrocalcinosis, cystic dilatation of renal calyces and a 4 mm obstructing stone without significant hydro.: 
Is this: 
Dent disease
Medullary Sponge Kidney 
Distal RTA
Barrter Syndrome
Primary Hyperparathyroidism
A

Medullary Sponge Kidney

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14
Q

What is medullary sponge kidney?

A

A congenital disorder characterised by cystic dilation of the terminal collecting ducts.
It is commonly associated with nephrocalcinosis and recurrent calcium stones.

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15
Q

Historically - how was medullary sponge kidney diagnosed?

A

IV pyelography which demonstrated pooling of contrast within the cystic dilation creating a characteristic appearance that may be compared to a paintbrush or a bouquet of flowers.
Ct Scanning without contrast can detect medullary nephrocalcinosis which is suggestive.

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16
Q

Why do patients with medullary sponge kidney get nephrolithiasis?

A

Urinary stasis within the dilated papillary ducts

But they also have additonal risk factors including hypercalciuria, hypocitraturia, and incomplete distal RTA.

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17
Q

True or False

Nephrocalcinosis commonly occurs in primary hyperparathyrodisim.

A

False - Very uncommon.

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18
Q

What is Dent disease?

A 
X linked recessive inheritance. 
Proximal tubular disorder
Characterised by hypercalciuria 
Low molecular weight proteinuria 
Nephrocalcinosis ( 75%) and  CKD

The first cases also were associated with hypophosphataemia.

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19
Q

How is iron deficiency defined in the haemodialysis population?

A

TSats <20%
Ferritin <200ng/mL

Relative iron deficiency that results in hyporesponsiveness to an erythropoiesis-stimulating agent (ESA)

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20
Q

What is hepcidin’s role in the anaemia of ESRD?

A

Chronic inflammation associated with ESRD results in increased production of the liver peptide hormone hepcidin. Hepcidin induces degradation of ferroportin, a protein responsible for the transport of iron out of enterocytes and other cells. This leads to iron trapping and a reduction in iron available for erythropoiesis. The administration of IV iron results in an increase in available iron, leading to an increase in hemoglobin concentration, and may reduce the required dose of erythropoietin.

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21
Q

Immediate adverse reactions to IV iron are generally attributed to -

A

Free iron content of the agent

Iron Sucrose (Venofer) and ferric gluconate have relatively high amounts of free iron so are given at low doses more frequently

Ferumoxytol and Ferric carboxymaltose(ferrinject) have lower amounts of free iron so theses are tolerated in larger doses.

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22
Q

Oral versus IV iron replacement for ESRD?

A

IV - “impaired gastrointestinal absoprtion of iron”
Randomized controlled trials and observational studies have demonstrated that oral iron fails to supply sufficient amounts of iron for erythropoiesis compared with IV iron preparations in patients with ESRD.

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23
Q

What is ferric pyrophosphate citrate?

A

Ferric pyrophosphate citrate is a water-soluble iron salt that is administered to patients through the dialysate. Compared with standard dialysate, dialysate with ferric pyrophosphate citrate decreases ESA dose requirements and improves iron stores. However, ferric pyrophosphate citrate does not completely obviate the need for IV iron supplementation. Although the slower delivery of iron with ferric pyrophosphate is more physiologic, prevents iron deficiency, and may avoid the potential hazards of IV iron, the role of this strategy in the management of symptomatic anemia is still unclear. At present, correction of iron deficiency with an IV preparation is preferred.

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24
Q

How does demeclocycline act?

A

Tetracycline derivative
Limits the collecting tubule responsiveness to ADH - an aeffect that can take several days to become apparent and then persists for several days.
Poorly tolerated due to nausea & vomiting.

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25
Q

What is tolvaptan and how does it act?

A

Tolvaptan, the only V2 receptor antagonist approved for use in the United States, is approved for the short-term treatment of hypervolemic or euvolemic hyponatremia refractory to fluid restriction
Expensive.

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26
Q

Can you use tolvaptan in patients with liver disease?

A

There is concern regarding the use of tolvaptan in patients with liver disease based on the observation of elevated liver enzyme levels in patients receiving tolvaptan compared with placebo in the Tolvaptan Efficacy and Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes (TEMPO) trial.

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27
Q

True/ False -

Asymptomatic hyponatraemia of 128 in a patient with cirrhosis warrants treatment

A

False.

No clear evidence of benefit of treating asymptomatic hyponatraemia in patients with chronic liver disease unless < 120.

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28
Q

Electrolyte abnormality following pancreatic transplant in the 1990s.

A

Chronic non -anion gap metabolic acidosis. Commonly seen in patients with exocrine drainage of pancreas allograft to the bladder.
1985 - 1999. Main benefit - able to identify rejection by measuring amylase in urine.
Most patients require exogenous bicarbonate therapy.
How do you treat? Surgical conversion to enteric drainage of the pancreas.
Be careful with DKA- will drain into urine.
Urinary dipstick measurement of protein is pH dependent - at high urinary pH will lead to a false positive.

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29
Q

What RTA is associated with calcineurin inhibitors?

A

Type 4 - Hyperkalaemia.

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30
Q

What combination of medications is least likely to precipitate post transplant diabetes mellitus in a patient with multiple predisposing risk factors?

A

Belatacept/ Mycophenolate/ Pred.

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31
Q

IgA nephropathy recurss in what % of transplant recipients?

A

Up to 60%

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32
Q

What % of patients develop Post Transplant Diabetes within 1 year of transplant ?

A

5 - 20% within 1 year of transplant

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33
Q

Greatest risk factors for post transplant diabetes mellitus

A

Age > 40
Obesity
Family History
African - American Race

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34
Q

What calcineurin inhibitor is most associated with PTDM

A

Tacrolimus

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35
Q

How do calcineurin ihibitors increase the risk of developing diabetes?

A

They inhibit insulin release.

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36
Q

How does Belatacept work?

A

It exerts an immunosuppresive effect by inhibiting T cell activation through costimulation blockade

In randomized controlled trials that compared belatacept-based regimens with CNI-based regimens, patients who received belatacept had a lower incidence of post-transplant diabetes.

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37
Q

Case: Pregnant woman with preeclampsia - Gets magnesium. She has a fistula. Is intubated. Mag is very high what do you do…

Haemodialysis
Ca gluconate.

A

Give IV calcium gluconate.

Mag is best option for seizures in eclampsia.
Patients with advanced CKD unable to excrete excess magnesium and are at risk of magnesium toxicity.

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38
Q

What are the symptoms of hypermagnesemia

A

Neuro effects: Diminished deep tendon reflexes, quadriplegia, somnolence and respiratory arrest.
CVS effects: Hypotension, bradycardia, complete heart block, cardiac arrest
ECG findings - PR interval prolongation, QRS widening, T wave amplitude changes, torsades de Pointe
May also cause hypocalcaemia by inhibiting PTH release.
May cause hyperkalaemia by prevention of the tubular potassium secretion.

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39
Q

Do you treat a pregnant woman with asymptomatic bacteriuria? If yes how

A

Amoxicillin 3- 7 days.

Alternative options for resistant organisms include cefpodoxime 100 mg twice daily for 3–7 days or fosfomycin 3 g as a single dose.

Occurs in 10% of pregnancy. Risk of leading to pyelo if untreated.

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40
Q

Can you give nitrofurantoin in the first trimester?

A

No.

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41
Q

Can you give septrin in the first trimester or near term?

A

No. Seems to be safe in mid pregnancy.

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42
Q

Can you give quinolones in the first trimester?

A

No. Risk of fetal malformation.

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43
Q

Why are patients of African Ancestry more likely to develop HIVAN and ESRD

A

They are more likely to carry two copies of the G1 and G2 alleles of APOL1, ( which offer protection against protection against trypanosoma brucei)

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44
Q

Does antiretroviral therapy stop progression of HIVAN to ESRD?

A

No.
ESRD still very likely with ART
Occurs in 60% of patients
With a median renal survival of 40 months.

45
Q

What are the biopsy findings of HIVAN?

A

Glomerular capillary collapse
Podocyte hypertrophy and proliferation
Intersitial fibrosis and oedema
Tubular microcystic dilation
EM frequently reveals endotherlial tubulreticular inclusions ( TRIs)
Kidneys appear large and markeldy echogenic by ulrtasound

TRIs may also occur inn lupus nephritis, look at complement levels.

46
Q

Symptoms of acute hypocalcaemia?

A

Neuromuscular excitability, causing tetany, paresthesia, larynogospasm, and focal and generalised seizures.
Cardiovascular complications - T wave alternans, prolonged QT interval, reversible congestive heart failure
Psychiatric complications: Depression, confusion, Psychosis
Papilledema and Optic neuritic have been reported.

Trousseau sign, carpal spasm induced by mild hypoxia from an inflated blood pressure cuff, is characterized by thumb adduction, wrist and metacarpophalangeal flexion, and interphalangeal extension. Chvostek sign is facial muscle spasm elicited by tapping the parotid gland over the ipsilateral facial nerve.

47
Q

Features of Zinc deficiency

A

Acrodermatitis enteropathica
Decreased taste and smell
Increased susceptibility to infections

48
Q

Features of hypophosphataemia

A

Impaired cardiac contracility

Increased susceptibility to ventricular arrhythmia

49
Q

Can levamisole cause ANCA vasculitis -

A

Levamisole has been implicated in numerous cases of ANCA vasculitis among cocaine users. Levamisole activates the subtype 3 muscarinic receptor on neutrophils, causing necrosis, release of intracellular contents, and formation of neutrophil extracellular traps (NETs).

50
Q

Features of ANCA vasculitis on biopsy

A

Crescents with fibrinoid necrosis

Minimal staining with immunofluorescence “pauci immune”

51
Q

Feature of anti GBM disease on biospy

A

Immunofluorescence show liner IgG staining along the GBM

52
Q

Features of Hepatitis C mediated MPGN on biopsy

A

Tram track appearance of the GBM, subepithelial and intramembranous immune complex depositis.
And possibly cyroglobulins on electron microscopy

53
Q

Features of Lupus Nephritis on biopsy

A

Lupus nephritis classically shows “full house” immunostaining (strongly positive for IgG, IgM, IgA, C3, and C1q);

54
Q

Approach to hypokalaemia questions…

A

Differentiate between renal and non renal losses.

Urine K excretion is determined by 24 hour urine collection, spot Urinary K, or Urinary K: Urinary creatinine ratio.

55
Q

True/ False

Urinary K: Urinary Cr < 15mmol/g suggests appropriate K conservation is the presence of hypokalaemia

A

True.

56
Q

How does hypomagnesemia cause hypokalaemia?

A

Hypomagnesemia depletes intracellular Mg++, which normally blocks K+ efflux through the renal outer medullary K+ (ROMK) channel, thus inducing renal K+ loss.

57
Q

How does cetuximab cause hypomagnesemia?

A

Hypomagnesemia in this case is caused by cetuximab, a monoclonal antibody against the epidermal growth factor receptor (EGFR). EGFR blockade downregulates transient receptor potential melastatin 6 (TRPM6), the dominant Mg++ channel in the distal nephron, inducing renal Mg++ loss. Hypomagnesemia actually predicts a beneficial chemotherapeutic response to agents such as cetuximab.

58
Q

41 yo HD patient ( ESRD 2 to diabetes) brought to ED with SOB + altered mental status. Family feel short term memory has deteriorated.
Unable to walk without falling.
Nystagmus, myoclonus, ataxia.

A

Thiamine deficiency.

Thiamine pyrophosphate is an essential enzyme cofactor in glycolysis (pyruvate dehydrogenase complex), the citric acid cycle (α-ketoglutarate dehydrogenase complex), and the pentose phosphate pathway (transketolase)

59
Q

Features of thiamine deficiency

A

Cardiovascular complications include high-output heart failure, as manifested by dyspnea, tachycardia, cardiomegaly, elevated pulse pressure, and pulmonary and peripheral edema. Neurologic manifestations may be acute (Wernicke encephalopathy) or chronic (Korsakoff syndrome) and include nystagmus, ophthalmoplegia, ataxia, confusion, confabulation, and impaired short-term memory. Thiamine deficiency may also cause type B lactic acidosis, which occurs when pyruvate is converted to lactate due to pyruvate and α-ketoglutarate dehydrogenase inhibition, nicotinamide adenine dinucleotide + H+ accumulation, and adenosine triphosphate depletion.

60
Q

Is thiamine deficiency more common in ESRD population and why?

A

Plasma thiamine levels decrease by 6% after HD. In addition, the erythrocyte concentration of oxythiamine, a transketolase inhibitor and putative uremic toxin, increases by 4-fold in patients receiving HD, which is correlated with a 41% decrease in erythrocyte transketolase activity.
Nutritional supplementation with water-soluble vitamins is recommended in ESRD. Thiamine, 100 mg orally daily, normalizes erythrocyte transketolase activity in patients undergoing maintenance HD.

61
Q 
Most important factor in choice of dialysis modality? 
PCKD
Obesity
Patient Preference
Prior open abdominal surgery
A

Patient Preference

62
Q

True/ False Prior abdominal surgery has not been shown to predict the extent of adhesions, and feasibility of PD and long term catheter survival is comparable between patients with and without prior surgery

A

True

63
Q

Considerations for ADPKD patients considering peritoneal dialysis

A

Higher risk of hernia formation and dialysate leaks related to increased intra- abdominal pressure.

But long term outcomes including patient and technique survival have been shown to be similar between patients with ADPKD and those with other causes of ESRD

64
Q 
Obesity's impact on PD outcomes - 
In terms of frequency of peritonitis. 
Hospitalisations
Hernias 
Survival
A

A retrospective cohort analysis of matched obese and nonobese patients receiving PD found that patients with BMI >34 tended to have earlier and more frequent peritonitis but experienced fewer hospitalizations, fewer hernias, and similar survival when compared with nonobese patients

65
Q

Differential for hypokalaemia and hypertension

A

Diuretic induced hypokalaemia (This is dose dependent - occurs in 7 - 8% of patients, usually in the first 2 weeks of therapy and is usually self limited - because there is a compensatory increase in potassium reabsorption + decreased secretion in the distal nephron. So long term thiazide use the answer is not the hypokalaemia)
Aldosterone excess
Conditions that mimic hyperaldosteronism (like secondary hyperaldosteronism due to occult renal artery stenosis)

66
Q

Does potassium effect intrepretation of an aldosterone result?

A

A normal serum potassium level is required to interpret aldosterone and renin screening values, as hypokalemia suppresses aldosterone secretion

67
Q

Secondary hyperaldosteronism due to occult renal artery stenosis - what renin result are you expecting?

A

Raised renin.

“However, most patients with renovascular hypertension would have increased, not decreased, renin activity, so this is not the most likely diagnosis in this patient with relatively well-controlled hypertension and suppressed plasma renin activity.”

68
Q

Mechanism of herbal tea causing hypokalaemia

A

In this case, ingestion of an “herbal tea” may be a clue. Many herbal products may contain licorice root for flavor, medicinal purposes, or both. These products may contain significant amounts of glycyrrhetinic acid. This compound produces mineralocorticoid excess effects by blocking 11-β-hydroxysteroid dehydrogenase type 2, leading to increased intracellular cortisol levels, which can activate the mineralocorticoid receptor. Glycyrrhetinic acid can also activate the mineralocorticoid receptor itself and block metabolism of aldosterone, producing further mineralocorticoid activity. Patients taking diuretics may be particularly susceptible to the hypokalemic effects and may also have a blunted hypertensive response

69
Q

What is “relapsing peritonitis”

A

This patient has relapsing peritonitis, which is defined as a second episode with the same organism within 4 weeks of completion of antibiotics for the initial episode

70
Q

What is repeat peritonitis?

A

Repeat peritonitis is another episode of peritonitis with the same organism >4 weeks after completion of antibiotics for the initial episode.

71
Q

What is recurrent peritonitis?

A

Recurrent peritonitis, defined as another episode of peritonitis with a different organism within 4 weeks of stopping antibiotics, is usually due to episodes of touch contamination with poor patient technique.

72
Q

What organisms are most likely to cause seeding from a biofilm?

A

Seeding from biofilm is especially common with coagulase-negative staphylococci but can also occur with Staphylococcus aureus, Pseudomonas aeruginosa, and other organisms.

73
Q

Antibiotic regimen for PD peritonitis that provides synergy -
Gram + and negative activity

A

Vanc and Ceftazidime

74
Q

Can icodextrin cause an aseptic peritonitis?

A

Icodextrin can cause an aseptic peritonitis, but this is rare. When this occurs, the peritoneal fluid cultures are negative.

But no differences in the risk for peritonitis have been shown in patients using icodextrin or a dextrose-containing dialysate

75
Q

What % of patients with ADPCKD have hepatic cysts?

A

> 70%

76
Q

What is medullary cystic kidney disease?

A

recently reclassified as autosomal dominant tubulointerstitial kidney disease (ADTKD), consists of a group of rare genetic disorders characterized by slowly progressive CKD with a bland urine sediment and minimal or no proteinuria. Medullary cysts may be seen on kidney ultrasound, but despite its previous name, they are not present in most cases. Hyperuricemia and recurrent gout, as well as anemia, are also common in some of the associated diseases

77
Q

Criteria for simulataneous liver- kidney transplant?

A

Liver transplant candidates who meet one of the following criteria are eligible for SLK:

  1. Diagnosis of CKD with a measured or calculated GFR of ≤60 mL/min/1.73 m2 for >90 consecutive days and at least one of the following at the time of waiting list registration:
    • ESRD on dialysis
    • Measured or calculated creatinine clearance or GFR ≤35 mL/min/1.73 m2
  2. Diagnosis of sustained AKI and at least one of the following for the last 6 weeks:
    • Dialysis at least once every 7 days
    • Measured or calculated creatinine clearance or GFR ≤25 mL/min/1.73 m2 documented at least once every 7 days
  3. Diagnosis of metabolic disease with an additional diagnosis of at least one of the following:
    • Hyperoxaluria
    • Atypical hemolytic-uremic syndrome from mutations in factor H or factor I
    • Familial non-neuropathic systemic amyloidosis
    • Methylmalonic aciduria
78
Q

Method of reducing catheter exit site infections from MSSA?

A

The application of mupirocin to the catheter exit site reduces the risk for catheter infection and bacteremia in patients receiving dialysis.

. The application of topical mupirocin ointment to the catheter exit site until healed was found to reduce the rate of bloodstream infection by approximately 85%.

79
Q

Do silver coated dialysis catheters work?

A

A 1998 study of silver-coated dialysis catheters found no reduction in the rate of CRBI and more reactions to the catheter that occasionally necessitated removal.

80
Q

In the presence of hypokalaemia and normal kidney function - what should the urine potassium concentration be?
And what should the urine to potassium creatinine ratio be?

A

In the presence of hypokalemia and normal kidney function, the urine potassium concentration should be <20 mEq/L

or a random urine potassium-to-creatinine ratio should be <25 mEq/g

81
Q

Impact of refeeding syndrome on potassium -

A

Thus, the decline in the serum potassium concentration is most likely due to a shift in potassium to the intracellular space. This is consistent with refeeding syndrome, a disorder that is characterized by severe electrolyte shifts in the setting of aggressive treatment of malnutrition.

82
Q

How to manage refeeding syndrome?

A

Nutritional repletion should be started slowly and individualized with a goal to meet nutritional requirements within 4–7 days. Patients should also receive thiamine and other vitamins before feeding begins. In addition, caregivers should closely monitor levels of potassium, phosphate, calcium, and magnesium and replete as needed.

83
Q

How do PPIs cause hypomagnesemia?

A

Proton-pump inhibitors such as pantoprazole can lead to significant hypomagnesemia because changes in the gastric pH limit absorption of magnesium by enterocytes.

84
Q

How do beta lactam antibiotics cause hypokalaemia?

A

β-lactam antibiotics can cause hypokalemia from urinary losses because these agents function as non-reabsorbable anions in the distal nephron.

85
Q

Does heparin cause hypokalaemia?

A

No - hyperkalaemia - Heparin can lead to hyperkalemia, not hypokalemia, because it limits aldosterone synthesis and can lead to hypoaldosteronism in patients with marginal aldosterone production

86
Q

Delay in treatment & recognition of a serious access infection - what should the medical director do?

A

Root Cause Analysis

One of the most important tools is root cause analysis, which uses such techniques as the fishbone diagram to delineate all the potential contributing causes that may have led to an adverse “effect.”.

87
Q

How do you calculate the urinary anion gap?

A

Urinary Sodium + Urinary Potassium - Urinary Chloride

88
Q

How do you evaluate polyuria?

What is the differential diagnosis for polyuria?

How do you calculate the daily urinary solute?

What is typical daily solute intake?

How do you distinguish difference between polydipsia and DI?

A

Polyuria - the first step is determine whether there is a water diuresis or solute diuresis.

Polyuria requires consideration of daily solute excretion.

The differential includes: central DI, nephrogenic DI, primary polydipsia and solute diuresis.

Urinary osmolality x urinary volume = daily urinary solute - which approximately daily solute intake (= total daily osmoles)

Their example is
267 mOsm/kg x 6L/d= 1602m0SM/D

Typical daily solute intake is approx 600 - 900mOsm/ day

In general, when the daily solute excretion is <600 mOsm, polyuria represents a water diuresis, and if >1000 mOsm, polyuria is the result of a solute diuresis.

A water deprivation test is performed to determine whether hyperosmolality can stimulate release of endogenous vasopressin to produce concentrated urine.

89
Q

How much protein should woman without CKD consume per day?

A

0.8/ kg/ day

90
Q

What effect does Gitelman syndrome have on serum potassium + urinary sodium, potassium?

A

Low serum potassium

Increased urinary Na
Increased urinary K

91
Q

How do you calculate contribution of urea to the daily solute excretion?

Urine urea: 32g/ 24 hours
6 L of urine.

A

32 divided by 6 = 5.3g/L or 530mg/dL urine urea nitrogen

Can be converted to mOsm/L by dividing by 2.8

So urea accounts for mOsm /l

92
Q

How do you calculate your protein intake?

A

(Urine urea nitrogen + (weight in kilograms x 0.031g nitrogen per kilo per day)) x 6.25

93
Q

What test should be performed in setting of recurrent nephrolithiasis and normal anion gap metabolic acidosis?

A

ANA

94
Q

Normal anion gap and urine pH is not maximally acidic. Is this suggestive of a distal or proximal RTA?

A

Suggestive of distal rather than proximal RTA.

Taken together, this should raise the concern for distal RTA rather than a proximal RTA because the urine can be maximally acid in the setting of proximal RTA when the serum bicarbonate value is below the bicarbonate resorptive threshold.

95
Q

What is the urinary anion gap in patients with a diarrhoeal acidosis?

A

The urine anion gap therefore is usually negative and in the -20 to -50 mEq/L range in patients with diarrheal acidosis

96
Q

What kidney stones are most likely to form in the setting of a distal RTA?

A

comprised of calcium phosphate. This is the result of several factors. There is increased release of calcium and phosphate from the buffering of acid by bone. The increased filtered load in the setting of a relatively high urine pH favors calcium phosphate precipitation. In addition, urinary citrate tends to be low in distal RTA because the persistent metabolic acidosis favors increased proximal reabsorption of citrate. Urinary citrate normally chelates calcium and increases its solubility.

97
Q

Differential for adult onset distal type 1 RTA?

A

Adult-onset distal (type 1) RTA can be a manifestation of autoimmune disorders such as Sjögren syndrome and SLE. It is therefore important to investigate these conditions in a patient who presents with otherwise unexplained distal RTA. Additional serologic testing, including anti-Ro/SSA and anti-La/SSB antibody testing, would be appropriate if the ANA result is positive or if Sjögren syndrome is strongly suspected, because SSA/SSB results may occasionally be positive despite a negative ANA result.

Sarcoidosis can cause a distal RTA.

98
Q

Can lead toxicity cause a distal RTA?

A

No - more likely to cause a proximal RTA.

Renal manifestations of lead toxicity include Fanconi syndrome, including proximal RTA, or CKD with hyperuricemia and minimal proteinuria.

99
Q

How do you diagnose cystinosis?

A

Instead, the diagnosis can be made by any of 3 methods: measuring the cystine content of peripheral blood leukocytes and fibroblasts; identifying a mutation in cystinosin, a lysosomal cystine transporter; or identifying corneal cystine deposits by slit lamp examination. Cystinosis causes proximal tubular dysfunction and proximal RTA. This condition usually presents in the first 3–6 months of life, although milder, late-onset (juvenile) and adult forms have been described. The adult form is primarily characterized by ocular manifestations.

100
Q

How do you do a water deprivation test?

A

Baseline data, including body weight, serum sodium, serum osmolality, and urine osmolality, are obtained. Then urine volume and body weight are measured hourly, and serum sodium, serum osmolality, and urine osmolality are measured every 2 hours. This process is continued until the urine osmolality reaches a plateau or serum osmolality exceeds 300 mOsm/kg.

101
Q

What test do you use to determine if hyperosmolality will stimulate the release of endogenous vaspopressin

A

Water Deprivation Test

102
Q

Administration of desmopressin in setting of central DI - what do you expect the urine osmolality to raise to?

A

> 600 mOsm/kg

An increase of 400 - 6000
An increase in urine osmolality to 400–600 mOsm/kg indicates a partial response and suggests an incomplete nephrogenic mechanism for the DI.

103
Q

If desmopressin is administered in the setting of polyuria and the urine osmolality does not increase to > 400 what is this indicative of

A

Nephrogenic DI

104
Q

What is copeptin?

A

Copeptin, a component of the precursor protein from which AVP is derived, is emerging as a more reliable marker to distinguish partial central DI from partial nephrogenic DI or primary polydipsia.

105
Q

Can oral contraceptive pills cause hypertension?

A

Oral contraceptive pills usually have a small effect on BP, but significant increases in BP and even severe hypertension can occur. This effect appears to be mediated primarily by estrogen in a dose-dependent manner, but some women are more susceptible. The mechanism is not well understood, but activation of the renin-angiotensin-aldosterone and sympathetic nervous systems have been implicated.

106
Q 
76 year old man - 
History of lithium use. 
Living in a care facility but ambulates with walker. 
Has water, tea and coffee served with each meal. 
Has Na: 153
Urine Na: 132
Urine Osmo: 852
What's the appropriate test? 
1. Water deprivation test 
2. MRI B 
3. Serum glucose measurement 
4. Vasopressin measurement
A

Ans: MRI B

Patient has hypernatraemia and hyperosmolality with an appropriately high urine osmolality. The high urine osmolality confirms that vasopressin is activated and effective in producing concentrated urine to conserve water.
But he has access to water -
So has an issue with thirst. Most likely explanation is hypodipsia - should have a MRI to look for a hypothalamic lesion.

107
Q

Features of autosomal dominant tubulointerstitial kidney disease

A 
Progressive loss of kidney function, 
bland urine sediment,
minimal proteinuria
Normal blood pressure 
Normal to small kidneys by ultrasound
Autosomal Dominant inheritance.
108
Q

Mutations in which genes are associated with autosomal dominant tubulointerstitial kidney disease

A
  • Uromodulin (UMOD)
  • Hepatocyte nuclear factor 1 B (HNF1B)
  • Renin (REN)
  • mucin 1 (MUC1)

Nephrology (10 decks)

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