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Flashcards in Nephrology - MTB Deck (323):
1

Best initial test in nephrology

- Urinalysis
- BUN/ Cr

2

Urinalysis measurements

- Protein
- WBC
- Red cells
- Specific gravity and pH
- Nitrites

3

Severe proteinuria

- means glomerular damage

4

Tamm-Horsfall protein

- tubules secrete slight amounts of protein
- less than 30 - 50 mg per 24 hrs

5

If there is persistent proteinuria

- not related to prolonged standing (orthostatic proteinuria), a kidney biopsy should be performed

6

Activities that increase urinary protein excretion

- Standing
- Physical activity

7

Normal protein per 24 hrs

< 300 mg

8

Assess proteinuria

- UA is the intial test
- Protein to creatinine ration is more accurate at determining the amount

9

Protein to creatinine ratio

1 is equivalent to one gram of protein on a 24 hr

10

Protein: creatinine ratio vs 24 hr urine

Protein: creatinine ratio can be superior in accuracy

11

Microalbunemia

- tiny amount of protein that is too small to detect on UA
- long term microalbinuria leads to worsening renal function in a diabetic patient should be treatment

12

Microalbunemia

- 30 - 300 mg/24 hrs

13

Diabetic patient is evaluated with a UA that shows no protein. Microalbuminuria is detected (level btwn 30 and 300 mg per 24 hrs). Next best step?

ACE inhibitors or angiotension receptor blocker
- best initial therapy for any degree of proteinuria in a diabetic patient

14

Is Bence-Jones protein in myeloma detectable on dipstick?

No. Use Immunoelectrophoresis

15

White blood cells on UA

- detect inflamation, infection, and allergic interstitial nephritis

16

Eosinophils

- indicate allergic or acute intersitial nephritiris

17

Detecting eosinophils in the urine

Wright and Hansel stains
- allergic intersitial nephritis
-

18

Hematuria

= / > 5 RBCs per high power field
- stones in bladder, ureter, or kidney
- hematologic disorders that cause bleeding (coagulopathy)
- infection (cystitis, pyelonephritis)
- cancer of bladder, ureters, or kidney
- tx ( cyclophosphamide gives hemorrhagic cysts)
- trauma
- glomerulonephritis

19

Ig A nephropathy

common for mild recurrent hematuria

20

Reason for false positive tests for hematuria

- Hemoglobin OR
- myoglobin

21

Woman is admitted to the hospital with trauma and dark urine. The dipstick is markedly positive for blood. Best initial test to conform the etiology?

Microscopic exam of the urine

22

Why is intravenous pyelogram is always wrong on boards?

- Slower and the contrast is renal toxic

23

When is dysmorphic red cells?

Glomerulonephritis

24

If the patient has hematuria without infection or prior trauma but
- Renal U/S or CT doesn't show etiology
- Bladder shows mass for possible biopsy

Next step?

Cystoscopy

25

Most accurate test of the bladder

Cystoscopy

26

Red cell casts in UA

Glomerulonephritis

27

White cell casts in UA

Pyelonephritis

28

Eosinophils casts in UA

Acute (allergic) interstitial nephritis

29

Hyaline casts in UA

Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitaes or concentrates into a cast

30

Waxy casts in UA

Chronic renal disease

31

Granular "muddy-brown" casts on UA

Acute tubular necrosis
- they are collections of dead tubular cells

32

Acute Kidney Injury

- formerly called acute renal failure
- decrease in creatinine clearance resulting in a sudden rise in BUN and creatinine

33

Three different types of AKI

- Prerenal azotemia (decreased perfusion)
- Postrenal azotemia (obstruction)
- Intrinsic renal disease (ischemia and toxins)

34

Prerenal azotemia

- due to inadequate perfusion of the kidney when kidney is normal
- hypotension
- hypovolemia
- renal artery stenosis

35

NSAIDS on afferent arteriole

- constrict the afferent arteriole

36

ACE inhibitors on efferent arteriole

- cause efferent arteriole vasodilation

37

Postrenal azotemia

- obstruction of any cause damages the kidney by blocking filtration at the glomerulus

38

Causes of postrenal azotemia

- PROSTATE HYPERTROPHY or cancer
- STONE in the ureter
- Cervical CANCER
- Urethral CANCER
- Neurogenic (atonic) bladder
- Retroperitoneal FIBROSIS

39

Causes of retroperitoneal fibrosis

- Bleomycin
- Methylsergide
- Radiation

40

Most common cause of intrinsic renal disease

Acute tubular necrosis
- from toxins and prolonged ischemia of the kidney

41

Other causes of intrinsic renal disease

- Acute (allergic) interstitial nephritis
- Rhabdomyolysis and hemoglobinuria
- Contrast agents, aminoglycosides, cisplatin,
- Crystals such as hyperuricemia, hypercalcemia
- Bence-Jones protein from myeloma
- Poststreptococcal infection

42

Clinical presentation of intrinsic renal disease

- Nausea and vomiting
- Tired/malaise
- Weak
- Short of breath and edema from fluid overload

43

Clinical presentation of severe intrinsic renal disease

- Arrhythmia from hyperkalemia and acidosis
- Sharp, pleuritic chest pain from PERICARDITIS

44

Clinical presentation of postrenal azotemia

- Enlargement (distention) of the bladder
- Massive diuresis after urinary catheter

45

Best initial test for acute kidney injury

- BUN : Cr

46

Prerenal azotemia

- BUN:CR > 20:1
- Clear hx of hypoperfusion and hypotension

47

Postrenal azotemia

- BUN:Cr > 20:1
- Distended bladder or massive release of urine with catheter placement AND bilateral or unilateral HYDRONEPHROSIS on U/S

48

Intrinsic renal disease

- BUN: Cr < 10:1

49

When is kidney biopsy the answer for AKI?

Never

50

Tests for AKI of unclear etiology

1. Urinanalysis
2.Urine sodium
3. Fractional excretion of sodium
4.Urine osmolality

51

Best test for AKI of unclear etiology

Urinalysis

52

Increased urine osmolality

- when intravascular volume is low, normally ADH levels should rise
- healthy kidney will reabsorb more water to fill vascularture
- increased water reabsorption leads to an increase in urine osmlolality -- more concentrated urine

53

Isosothenuria (same osmolality to the blood ~ 300 mOsm/L) or Low urine osmolality

- During ATN, the urine cannot be concentrated because the tubules cells are damaged

54

Urine osmolality: Healthy person with fluid overload

Low urine osmolality or dilute urine

55

Urine osmolality: Health person with dehydration

High urine osmolality or concentrated urine

56

20 y/o African American man comes for a screening test for sickle cell. He is found to be heterozygous (trait or AS) for sickle. Best advice for him?

Avoid dehydration
- sickle cell trait in renal concentrating ability or isosthenuria

57

Prerenal azotemia

- BUN:Cr > 20:1
- Urine Na < 20mEq/L
- Fractional excretion of sodium: < 1%
- Urine osmolality: > 500 mOsm/kg

58

Acute tubular necrosis

- BUN: Cr < 20: 1
- Urine Na > 20mEq/L
- Fractional excretion of sodium: >1%
- Urine osmolality: < 300mOsm/kg

59

Acute Tubular Necrosis

- an injury to the kidneys from ischemia and/or toxins resulting sloughing off of tubular cells into the urine
- Sodium and water reabsorptive mechanisms are lost with the tubular cells
- Proteinuria is not significant since protein, not tubule, spills into the urine

60

Urine specific gravity correlates to urine osmolality

- High UOsm = high specific gravity

61

Pt has acute renal failure and a toxin. What is the most likely diagnosis?

Acute Tubular Necrosis

62

Pt comes with fever and acute, left lower quadrant abdominal pain. Blood cx on admission grow E.coli and Candida albicans She is started on vancomycin, metronidazole, and gentamicin, and amphotericin. She has a CT scan that identifies diverticulitis. After 36 hrs, her creatinine rises dramatically. Most likely cause of her renal insufficiency?

Contrast media
- rapid onset of injury

63

Timeline for nephrotoxic drugs

Drugs (e.g. vancomycin, gentamicin, and amphotericin)
are nephrotoxic
- usually takes 5 to 10 days to result in nephrotoxicity

64

74 y/o blind man is admited with obstructive uropathy and chest pain. He has a hx of hypertension and diabetes. His creatinine drops from 10mg/dL to 1.2 mg/dL 3 days ater catheter placement. The stress test show reversible ischemia. Most appropriate management?

Saline hydration is has the most proven benefit at prevent contrast-induced nephrotoxicity

65

Pt with mild renal insufficiency undergoes angiograpy and develops 2mg/dL rise in creatinine from ATN despite the use of saline hydration before and after the procedure. What do you expect to find on lab testing?

Urine sodium 5 (very low), FENA

66

Pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises. Most likely cause?

Hyperuricemia
- most likely from tumor lysis syndrome
- cisplatin (drug toxicities) would not produce RISE in CREATININE In 5-10 days

67

Prevention of tumor lysis syndrome

- Allopurinol, hydration, and rasburicase should be given prior to chemotherapy to prevent renal failure from tumor lysis sndrome

68

Pt who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalysis shows an abnormality. What did she take?

Ethylene glycol
- AKI based on oxalic avid and oxalate precipitating within the kidney tubules cause ATN
- envelope shaped crystals

69

Drug-induced ATN

- nonoliguric renal injury caused by aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir, and cyclosporine
- slower onset: FIVE to TEN days
- dose dependent

70

What electrolyte deficiency predisposes someone to drug-induced aminoglycosides?

Low magnesium levels
- may increase risk of aminoglycosides or cisplatin toxicity

71

Contrast media nephrotoxicity

- can cause immediate renal toxicity
- prevented with saline hydration
- n-acetylcysteine and sodiu bincarbonate proven beneficial

72

Rhabdomyolysis

- caused by TRAUMA, prolonged IMMOBILITY, snake bites, seizures, and CRUSH INJURIES
- best initial test to confirm UA

73

Hyperuricemia

- ATN
- usually from tumor lysis syndrome
- long standing hyperuricemia from gout can cause chronic renal failure

74

Best initial to confirm the diagnosis of rhabdomyolysis

UA
- positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination

75

Reasons for false positive urine dipstick

Urine dipstick can't tell the difference between:
- Hemoglobin
- Myoglobin
- Red blood cells

76

Bence Jones protein

- directly toxic to renal tubules

77

Rhabdomyolysis: lab findings

- ELEVATED CPK - lets you know "hematuria" is myoglobin
- HYPERKALEMIA due to release of K from damaged cells
- HYPERURICEMIA due to degradation of nucleic acid from damaged cells
- HYPOCALCEMIA due to increased calcium binding to damaged muscle

78

Rhabdomyolysis: treatment

- SALINE HYDRATION
- MANNITOL as an osmotic diuretic
- BICARBONATE which drives K back into cells and prevent precipitation of myoglobin

79

Do you treat hypocalcemia in rhabdomyolysis?

No, if patient is asymptomatic.
- in recovery, the calcium will come back out of muscles

80

A man comes to ED after a triathlon, followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and the urine is dark. IV fluids are started . What is the next step?

EKG
- to detect life threatening hyperkalemia
** potassium replacement in a person with rhabdomyolysis would be fatal**

81

Rhabdomyolysis proven to benefit ATN

- No therapy proven to benefit ATN
- diuretics increase urine output, but do not change overall outcome

82

Wrong answers for treatment of ATN

- Low-dose dopamine
- Diuretics
- Mannitol
- Steroids

83

Indications for dialysis

- Fluid overload
- Encephalopathy
- Pericarditis
- Metabolic acidosis
- Hyperkalemia

84

BUN:Cr indications for dilaysis

- No specific level of BUN:Cr
- based on development of life threatening conditions

85

Hypocalcemia symtpoms

- Seizures
- prolonged QT interval leading to arrhythmia

86

Patient develops from ATN from gentamicin. She is vigorously hydrated and treated with high doses of diuretic, low dose dopamine, and calcium acetate as a phosphate binder. Urine output increases but she still progresses to end-stage renal failure. She also becomes deaf. What causes her hearing loss?

Furosemide
- causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss

87

Hepatorenal syndrome

renal failure developing secondary to liver disease
- kidneys are intrinsically neural

88

Hepatorenal syndrome: Hx and PE

- severe liver disease (CIRRHOSIS)
- new-onset renal failure w/ no other explanation
- VERY LOW URINE NA (less than 10 - 15 mEq/L)
- FENA < 1%
- ELEVATED BUN:Cr > 20:1

89

Hepatorenal syndrome: Treatment

- Midodrine
- Octreotide
- Albumin (albumin is less clear)

90

Atheroemboli: Etiology

- CHOLESTEROL PLAQUES found in aorta and/or coronary arteries can be "broken off" manipulated during catheter procedures
- CHOLESTEROL EMBOLI lodged in kidney causes AKI
- BLUE/PURPLISH SKIN LESIONS in fingers and toes, LIVEDO RETICULARIS and ocular lesions

91

Peripheral pulses in atheroemboli

- cholesterol plaques are too small to occlude vessels such as the radial or brachial artery

92

Atheroemboli: diagnostic tests

- Eosinophilia
- Low complement levels
- Eosinophiluria
- Elevated ESR

93

Most accurate diagnostic test for atheroemboli?

- Biopsy of one purplish skin lesions
- cholesterol crystals, but this result does not change management b/c there is no specific therapy to reverse atheroembolci disease

94

Acute (Allergic ) Interstitial Nephritis

- is a form acute renal failure that damages the tubules occurring on idiopathic issues
- antibodies and EOSINOPHILS ATTACK THE CELLS LINING THE TUBULES as a rxn to the drugs (70%), infxn, and autoimmune disorders

95

Most common cause of acute (allergic) interstitial nephritis

- PENICILLINS and cephalosporin
- SULFA DRUGS
- Phenytoin
- Rifampin
- Quinolones
- Allopurinol
- Proton Pump Inhibitors

96

Medications that cause AIN are that same as those cause:

- Drug allergy and rash
- Stevens-Johnson syndrome
- Toxic epidermal necrolysis
- Hemolysis

97

Acute (Allergic) Interstitial Nephritis: Clinical Presentation

- FEVER (80%)
- RASH (50%)
- Arthralgias
- Eosinophilia and EOSINOPHILURIA (80%)

98

Aside from drugs, other causes of AIN

Autoimmune diseases (e.g. SLE, Sjorgen, and sarcoidosis)

99

AIN Diagnostic Tests

- Elevated BUN: CR < 20:1
- White and red cells in the urine

100

Most accurate test for acute (allergic) interstitial nephritis

- Hansel or Wright stain determines whether eosinophils are present

101

Acute interstitial nephritis: treatment

AIN usually resolves spontaneously w/ stopping the drug or controlling the infection

102

Analgesic Nephropathy

- ATN from direct toxicity to the tubules
- AIN
- MEMBRANOUS GLOMERULONEPHRITIS
- VASCULAR INSUFFICIENCY
- PAPILLARY NECROSIS

103

Vascular insufficiency induced analgesic nephropathy

- INHIBIT PROSTAGLANDINS
- NSAIDS inhibit prostaglandins to constrict afferent arteriole and decrease renal perfusion

104

Papillary necrosis

- sloughing off of the renal papillae
- caused by toxins such as NSAIDS, or sudden vascular insufficiency leadingot death of cells in the pappillaw

105

Papillary necrosis: Hx and PE

- patient loses 60 - 70% renal function before the creatinine even begins to rise
- Look for extra NSAID use with a hx of:
- SICKLE CELL DISEASE
- Diabetes
- Urinary obstruction
- Chronic pyelonephritis

106

Papillary necrosis: Clinical presentation

- sudden onset of flank pain, fever, and hematuria in a patient with one of the diseae perviously list

107

Best initial test for suspected papillary necrosis

Urinanalysis
- grossly visible NECROTIC MATERIAL passed IN THE URINE

108

Most accurate test for papillary necrosis

CT scan
- shows the abnormal internal structures of the kidney from the loss of the papillae

109

Papillary Necrosis: Treatment

No specific therapy

110

Pyelonephritis

- onset in a few days
- Sx: dysuria
- Urine cx: positive

111

CT findings of pyelonephritis

Diffusely swollen kidney

112

Pyelonephritis: Treatment

Antibiotics
- such as ampicillin/gentamicin or fluoroquinolones

113

Papillary necrosis

- onset in a few hours
- necrotic material in urine
- negative urine culture

114

Papillary necrosis: treatment

No treatment

115

Tubular Disease: Overview

- Acute
- Toxins
- None nephrotic
- No biopsy usually
- No steroids
- Never additional immunosuppressive agents

116

Tubular Disease: Treatment

- Correcting HYPOPERFUSION and REMOVING TOXIN

117

Glomerular Diseases

- generally chronic
- not caused by toxins or hypoperfusion
- all of them can cause nephrotic syndrome
- biopsy indicated
- treated with steroids
- additional immunosuppresive medications

118

Most accurate diagnostic test for glomerular disease

- Steroids

119

Main difference between glomerulonephritis and nephrotic syndrome

Degree or AMOUNT of proteinuria

120

Diagnostic tests for glomerulonephritis

- UA with HEMATURIA
- "DYSMORPHIC" red cells
- RED CELL CASTS
- Urine sodium and FENA are low
- PROTEINURIA

121

Goodpasture Syndrome

- presents with LUNG AND KIDNEY involvement
- no UPPER RESPIRATORY TRACT INVOLVEMENT
- no skin, joint, GI, eye, or neurological involvement

122

Best initial test for Goodpasture Syndrome

- Antiglomerular basement membrane antibodies

123

Most ACCURATE test for Goodpasture Syndrome

- Lung or kidney biopsy with "LINEAR DEPOSITS"
- anemia is often present from chronic blood loss from hemoptysis

124

Goodpasture Syndrome: Treatment

- Plasmapheresis and steroids

125

IgA Nephropathy

- most common cause of acute glomerulonephritis in US
- look for Asian patient w/ recurrent epsiodes of gross hematuria 1 - 2 days after upper respiratory tract infxn
- poststreptococcal glomerulonephritis follows pharyngitis by 1 -2 weeks

126

Most accurate test for IgA nephropathy

Kidney biopsy
** IgA levels are increased in 50%**

127

Proteinuria and progression of disease

More proteinuria = worse progression

128

IgA Nephropathy

- no treatment proven to reverse the disease
- severe proteinuria is treated with ACE inhibitors and steroids

129

Postinfectious Glomerulonephritis

- most common organism leading to infectious glomerulonephritis is Streptococcus
- follows throat infectiou or skin infection (impetigo) by 1 to 3 weeks

130

Postinfectious Glomerulonephritis: Clinical Presentation

Patients present with:
- dark (cola-colored) urine
- periorbital edema
- hypertension
- oliguria

131

Postinfectious Glomerulonephritis: Diagnostic Tests

UA with proteinuria, red cells, red cell casts
- low complement

132

Pt had infection 2 weeks ago and is c/o dark urine, facial edema, and oliguria. Next step?

ASO titers and anti-DNAse antibod

133

Most accurate test for postinfectious glomerulonephritis

Kidney biopsy

134

Postinfectious glomerulonephritis: Treatment

Supportive treatment such as:
- antibiotics
- diuretics to control fluid overload

135

Alport Syndrome

congenital defect of type I collagen that results in glomerular disease combined with:
- sensorineural hearing loss
- visual disturbance from loss of the collagen fibers that hold lens of eye in place

136

Alport Syndrome: Treatment

No specific therapy to reverse defect

137

Polyarteritis Nodosa

systemic vasculitis of small and medium sized arteries that commonly affect kiney
- SPARES THE LUNG
- ASSOCIATED WITH HEPATITIS B

138

Why do patients with PAN have neuropathy?

Damage to small blood vessels around nerves starve them into neuropathy

139

Polyarteritis Nodosa: Clinical Presentation

Nonspecific symptoms of: fever, malaise, weight loss, mya;gias, and arthralgia

GI: abdominal pain, pain worsened by eating due to mesenteric ischemia

Neurologic: "mononeuritis multiplex" when damage occurs around large peripheral nerve (brachial, radial, ulnar)

Skin: purpura (large), petechiae (small), digital gangrene, livedo reticularis

140

Young patient has a stroke or MI.

Think vasculitis
- PAN

141

Polyarteritis Nodosa: Diagnostic Tests

Blood tests will show:
- anemia and leukocytosis
- elevated ESR and C-protein
- ANCA NEGATIVE
- ANA and rheumatoid

Angiography

142

Best diagnostic for polyarteritis nodosa

ANGIOGRAPHY of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset w/ HTN

143

Most accurate test for polyarteritis nodosa

Biopsy

144

POlyarteritis Nodosa: Treatment

Prednisone
Cyclophosphamide
- treat Hep B when found

145

Lupus Nephritis

- SLE can give any degree of renal involvement
can present with normal or mild proteinuria
- severe disease presents with membranous glomerulonephritis

146

Most accurate test for lupus nephritis

Biopsy
- will show glomerulosclerosis which has no active inflammatory component
- helps determine therapy based on stage

147

Lupus Nephritis: Treatment

Glucocorticoids combined with either cyclophosphamide or mycophenolate

148

Which conditions give LARGE kidneys on sonogram or CT scan?

- Amyloid
- HIV
- Nephropathy
- Polycystic kidneys

149

Amyloidosis

Abnormal protein produced in association with:
- myeloma
- chronic inflammatory diseases
- rheumatoid arthritis
- inflammatory bowel disease
- chronic infections

150

Most accurate test for amyloidosis

Biopsy
- show green birefringerence with Congo red staining

151

Amyloidosis: Treatment

Melphalan and prednisone

152

Nephrotic Syndrome

- measure of the severity of proteinuria in association with glomerular disease
- Massive proteinuria leads to:
- edema
- hyperlipidemia
- thrombosis: urinary anticoagulants protein C, protein S, and antithrombin

153

Nephrotic Syndrome: Etiology

Diabetes and HTN are most common causes of nephrotic syndrome

154

Nephrotic Syndrome associated with cancer (solid organ)

Membranous

155

Nephrotic syndrome associated with children

Minimal change disease

156

Nephrotic syndrome associated with drug use and AIDS

Focal segmental

157

Nephrotic syndrome associated with SLE

All types of nephrotic syndrome

158

Major difference between nephritic syndrome and nephrotic syndrome

Amount of proteinuria

159

Nephrotic syndrome: clinical presentation

Generalized edema

160

Why are infections more common with nephrotic syndrome?

Increased urinary loss of immunoglobulins and complement

161

Why are patients more clot prone with nephrotic syndrome?

Loss of antithrombin, protein C, and protein S

162

Best initial test for suspected nephrotic syndrome?

Urinalysis
- wil show Maltese crosses, which are lipid deposits from sloughed off tubular cells

163

Urine albumin/creatinine ration

- measure of the average protein produced over 24 hrs
- ratio of 2:1 means 2 grams of protein excreted over 24 hrs

164

Most accurate test to detect nephrotic syndrome

Renal biopsy

165

Nephrotic Syndrome: definition

Hyperproteinuria (> 3.5 g per 24 hrs)
Hypoproteinemia
Hyperlipidemia
Edema

166

Best initial therapy for nephrotic syndrome

Glucocorticoids
- if no response after several weeks, immunosuppresive meds such as cyclophosphamide

167

How are ACE inhibitors and ARBs used in nephrotic syndrome?

Try to control proteinuria

168

How is edema managed in nephrotic syndrome

Salt restriction and diuretics

169

How is hyperlipidema managed in nephrotic syndrome

Statis

170

End Stage Renal Disease

- kidney failure so sever as to need dialysis
- no defined as a particular BUN or creatiinine

171

Most common cause of end stage renal disease

Diabetes
Hypertension

172

ESRD: Clinical Presentation

Uremia in the presence of:
- metabolic acidosis
- fluid overload
- encephalopathy
- hyperkalemia
- pericarditis

173

Manifestations of Renal Failure

- Anemia
- Hypocalcemia and osteomalacia
- Bleeding
- Pruritis
- Hypoerphosphatemi
- Hypermagnemias
- Atherosclerosis
- Endocrinopathy

174

Renal Failure: Anemia

- loss of erythropoietin leads to monochromic anemia
- treat with erythropoietin and Fe supplements

175

Renal Failure: hypocalcemia

- less active 25- hydroxy-vitamin D into the much more active 1,25 dihydroxy vitamin D
-without 1,25 dihydroxy form of vitamin D, body will not absorb enough Ca from gut
- treat with vitamin D and calcium

176

Renal Failure: osteodystrophy

Low calcium leads to secondary hyperparathyroidism
- high parathyroid levels remove Ca from bones, making them soft and week

177

Bleeding 2/2 bleeding

Platelets do not work normally in uremic enviroment
- treat with DDVAP increases platelet function; use only when bleeding

178

Infection 2/2 renal failure

Neutrophils do not work because they cannot degranulate

179

Pruritis 2/2 renal failure

Urea accumulating in skin causes itching
- treat with dialysis and UV light

180

Hyperphosphatemia 2/2 renal failure

Phosphate normally excreted throgh kidneys. High parathyroid levels release phosophate from bones, but body is unable to excrete
- treat with oral binders

181

Hypermagnesmemia 2/2 renal failure

- loss of excretory ability
- treat with high Mg foods, laxatives, and antacids

182

Accelerated atherosclerosis and hypertension 2/2 renal failure

Immune system keeps artery clear of lipid acculiaton
WBCs dont work in uriemic environment - common cause of death in dialysis patients
- treat with dialysis

183

Endocrinopathy 2/2 renal failure

Women are anovulatory and men have low testosterone
- treat with dialysis, estrogen (women ) and testosterone (men ) replacement

184

Erectile dysfunction 2/2 renal failure

Insulin level tend to go up because insulin is excreted renally Insulin resistance also increases. Glucose leels are therefore up and down

185

Treatment of hyperphosphatemia

Oral phosphate binders
- prevent reabsorption of phosphate from bowe
- treat hypocalemia eill b/c it is hyperparathyroidsm that causes increase phosphate release from bone

186

When treating hypocalcemia why should you give oral phosphate binders?

If you use Vitamin D alone without oral phosphate binder then bowel will absorb increase GI absorption of phosphate

187

Why do you never use aluminum phosphate binders?

Aluminum causes dementia

188

Thrombotic Thrombocytic Purpura

platelet disorder in which microthrombi block small vessels leading to end organ ischemia .
RBCs are fragmented by microthrombi leading to microangiopathic hemolytic anemia

189

TTP associated conditions

HIV
Cancer
Drugs (cyclosporine, ticlopidine and clopidogrel)

190

TTP presentation

Clinical syndrome with 5 symptoms (3 of 5)
- low platelet
- microangiopathic hemolytic anemia
- neuro changes (seizures, stroke, delirium)
- impaired renal function
- fever

191

How is TTP hemolysis visible on smear?

Schistocytes
Helmet cells

192

Hemolytic Uremic Syndrome

- common in children
- associated with E.coli 0157:H7 and Shigella
- intravascular hemolysis (schistocytes)
- renal failure
- thrombocytopenia

193

TTP Treatment

Plasmaphoresis
** if not a choice, choose fresh frozen plasma
** NEVER CHOOSE PLASMA INFUSION

194

HUS: Treatment

Often resolves spontaneously

195

Simple renal cysts

- echo free
- smooth thin walls
- sharp demarcation
- good transmission to the back

196

Complex renal cysts

- mixed echogenecity
- thick, irregular walls
- lower density on back wall with demarcation
- transmission shows debris in cyst

197

Polycystic Kidney Disease

presents with:
- pain
- hematuria
- stones
- infection
- hypertension

198

What is the most common cause of death from PCKD?

Renal failure
- from recurrent episodes of pyelonephritis and nephrolithiasis

199

Conditions associated with PCKD

- liver cysts (most common site outside of kidney)
- ovarian cysts
- mitral valve prolapse
- diverticulosis
- berry aneurysms

200

Hypernatremia

due to loss of free water
- sweating, burns, fever
- pneumonia: insensible losses from hyperventilation
- diarrhea
- diuretic

201

Diabetes insipidus

- leads to high volume water losss from insufficient or ineffective ADH

202

Central diabetes insipidus

- can be caused by CNS disorders (stroke, tumor, trauma, hypoxia, infection) can damage ADH production in hypothalamus or storage in posterior pituitary
- low ADH

203

Nephrogenic diabetes insipidus

- loss of ADH effect on collecting duct of the kidney
- can be caused by lithium or demecycline, CKD, hypokalemia, or hypercalcemia
- elevated ADH

204

Pt has high volume nocturia

Think about presence of diabetes insipidus

205

Diabetes insipidus: presentation

DI w/ hypernatremia presents with neurological symptoms such as:
- confusion
- disorientation
- lethargy
- seizures

206

Complications of diabetes insipidus

If uncorrected, severe hypernatremia causes coma and irreversible brain damage

207

Polyuria

- high urine volume

208

Hypernatremia: diagnostic test

hyperosmolality
fluid losses from skin, kidney, or stool lead to:
- decreased urine volume
- increased urine osmolality
- decreased urine sodium

209

Diabetes Insipidus: Diagnostic Test

- high urine volume in DI
- decreased urine osmolality in DI

210

Best initial test for diabetes insipidus

Water deprivation then observation of urine output and urine osmolality
- In DI, high volume urine and low urine osmolality

211

Central diabetes insipidus response to ADH

Sharp decrease in urine volume, increase in osmolality

212

Nephrogenic diabetes insipidus response to ADH

No change in urine volume or osmolality with ADH administration

213

Positive water deprivation

means urine volume stays high despite withholding water

214

Diabetes inspidus: Treatment

1. Fluid loss: correct underlying water loss
2. CDI: replace ADH
3. NDI
- correct potassium and calcium
- stop lithium and demeclocycline
- give thiazide or NSAIDs despite these interventions

215

Complications of hypernatremia

Cerebral edema -- if sodium levels brought down too rapidly from shift of fluids from vascular space into cells of brain
- presents with worsening confusion and seizures

216

Hyponatremia

- characterized according to overall VOLUME STATUS of the body

217

Hypervolumia hyponatremia: causes

- CHF
- Nephrotic syndrome
- Cirrhosis

218

Intravascular volume depletion in regards to ADH levels

Increased ADH levels
- pressure receptors in atria and carotid sense decrease in volume and stimulate ADH production and release

219

Hypovolemia hypernatremia: causes

- Sweating
- Pneumonia: due to secondary losses from hyperventilation

220

Addison disease

- loss of adrenal function also causes hyponatremia b/c of loss of aldosterone
- less aldosterone, less sodium

221

Euvolemia hyponatremia: causes

- Pseudohyponatremia (hyperglycemia)
- Psychogenic polydipsia
- Hypothyroidism
- Syndrome of inappropriate ADH

222

Hyperglycemia induced hyponatremia

- very high glucose levels lead to a decrease in soidum levels
- hyperglycemia acts an osmotic draw on fluid inside the cells

223

Na correction with hyperglycemia

For every 100 mg/dL of glucose above normal, there is a 1.6 mEq/L decrease in Na

224

Psychogenic polydipsia

massive ingestion of free water above 12 to 24 liters/day will overwhelm kidney's ability to excrete water
- minimum urine 50 mOsm/kg
- can produce 12 - 24 liters of urine a day, depending whether or not you can get urine osmolality down to 50 or 100 mOsm/kg

225

Pt is hyponatremic with a hx of bipolar disorder. Likely diagnosis?

Psychogenic polydipsia

226

Hypothyroidism induced hyponatremia

- thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased

227

SIADH induced hyponatremia

Any LUNG or BRAIN DISEASE can cause SIADH for unclear reasons
- certain drugs: SSRIs, sulfonyureia, vincristine, cyclophosphamide

228

Cancers associated with SIADH

Small cell cancer of the lung produce ectopic ADH

229

Hyponatremia presentation

Presents entirely with CNS symptoms
- confusion
- lethargy
- disorientation
- seizures
- coma

230

Hyponatremia: Diagnostic Test

SIADH - urine is appropriately concentrated (high urine osmolality)
- urine sodium is high in SIADH
- uric acid level and BUN are low in SIADH

231

Most accurate test for SIADH

high ADH level

232

Mild hyponatremia: treatment

restrict fluids

233

Moderate hyponatremia: treatment

Saline and loop diuretic
* pt may present with minimal confusion

234

Severe hyponatremia: treatment

* patient presents with lethargy, seizures, coma
- treat with hypertonic saline, conivaptan, tolvaptan

235

ADH antagonists

Tolvaptan and conivaptan
- treated for severe, symptomatic SIADH

236

Chronic SIADH

- can be from underlying disorder that cannot be corrected (e.g. metastatic cancer)

237

Chronic SIADH: treatment

Demeclocycline
- blocks the action of ADH at the collecting of the kidney tubule

238

Hyponatremia complications

Central pontine myelinolysis
- must be corrected "slowly" as under 0.5 - 1.0 mEq/hr or 12 to 24 mEq per day

239

Pseudohyperkalemia

Falsely elevated potassium levels due to:
- hemolysis
- repeated fist clenching with tourniquet
- thrombocytosis or leukocutosis will leak out of cells in the lab specimen

240

Hyperkalemia due to decreased excretion

- Renal failure
- Aldosterone decrease
- ACE inhibitors/ ARBS
- type IV renal tubular acidosis
- spironolactone and eplerenone (aldosterone inhibitors)
- triamterene and amiloride (K sparing diuretics)
- Addison disease

241

Hyperkalemia due to K release from ittuse

- Tissue destruction (hemolysis, rhabdomyolysis, tumor lysis syndrome)
- Decreased insulin (insulin drive K into cells)
- Acidosis: cells take in H+ and release K in exchange
- Beta blockers and digoxin: drugs inhibit Na/K ATPase
- Heparin increases K levels, presumable through increased tissue release

242

Hyperkalemia: presentation

K disorders interfere with muscle contraction and cariac conductance
- weakness
- paralysis when severe
- ileus (paralyzes gut muscles)
- cardiac rhythm disorders

243

Best initial test for hyperkalemia

EKG

244

Hyperkalemia: EKG findings

Peaked T waves
Wide QRS
PR interval prolongation

245

Treatment for life threatening hyperkalemia

1. Calcium chloride or calcum gluconate
2. Insulin and glucose to drive potassium back into cells
3. Bicarbonate: drive potassium into cells but should be used most when acidosis causes hyper

246

Removing potassium fro body

Kayexalate (sodium polystyrene sulfonate) removes potassium from body through bowel
-

247

Other methods to lower potassium

- Inhaled beta agonists
- Loop diuretics
- Dialysis

248

When there is hyperkaelmia and an abnormal EKG, what is the most appropriate next step?

Calcium chloride or calcium gluconate

249

Hypokalemia

- due to decreased intake
- shift in to cells
- renal loss
- hypomagnesmia
- renal tubular acidosis

250

Hypokalemia 2/2 shift into cells

- Alkalosis (H+ ions come out cell in exchange for K)
- Increased insulin
- Beta adrenergic stimulation (accelerates Na/K ATPase)

251

Hypokalemia 2/2 renal loss

- Loop diuretics
- Increased aldosterone
- Primary hyperaldosteronism (Conn syndrome)
- Volume depletion raises aldosterone
- Cushing syndrome
- Bartter syndrome (genetic disease causing salt loss in Loop of Henle)
- Licorice

252

Hypokalemia 2/2 hypomagnesmia

There are Mg-dependent K channels. When magnesium is low, they open and spill potassium in the urine

253

Hypokalemia 2/2 GI loss

- seen in vomiting, diarrhea, and laxative abuse

254

Hypokalemia presentation

Leads to issue with muscular contraction and cardiac conduction
- Weakness
- Paralysis
- Loss of reflexes

255

Hypokalemia EKG findings

U waves are the most characteristics
- ventricular ectopy (PVCs)
- flattened T waves
- ST depression

256

Hypokalemia: treatment

No maximum rate of oral K replacement
- however with rapid IV potassium replacement, it can cause arrhythmia

257

PT is admitted with vomiting and diarrhea from gastroenteritis. His volume status is corrected with IV fluids and the diarrhea resolves. His pH is 7.40 and his serum bicarbonate has normalized. Despite oral and IV replacement, his potassium level fails to rise. What should you do?

Check magnesium level
- hypomagnesmia can be lead to increased urinary loss of K

258

A woman with ESRD and G6PD deficiency skips dialysis for a few weeks and then is crushed in a MVA. She taking dapsone and has recently eating a few fava beans. What is the most urgent step?

EKG
if abnormal, give patent Ca chloride

259

Renal Tubular Acidosis

metabolic acidosis with a normal anion cap (6 - 12)

260

Two most important causes of metabolic acidosis with normal anion gap

- RTA
- Diarrhea

261

Why is the anion gap normal in RTA and diarrhea

Chloride level rises 2/2 they are also refer to hyperchloremic metabolic acidosis

262

Anion gap metabolic acidosis

due to ingested substances:
- ethylene glycol or methanol
- organic acids (e.g. lactate) that are anion and drive down chloride level

263

Distal RTA (Type I)

- distal tubule is responsible for generating new bicarbonate under the influence of aldosterone
- increased formation of kidney stones from calcium oxalate 2/2 alkaline urine
- calcifies the kidney parenchyma

264

Drugs that cause distal RTA (Type I)

- Amphotericin
- Autoimmune disease (e.g. SLE or Sjorgen syndrome can damage distal tubule)

265

Best initial test for Distal RTA

Urinalysis
- looking for an abnormally high pH > 5.5

266

Most accurate test for Distal RTA

- infuse acid into the blood with ammonium chloride

267

Treatment of Distal RTA

Replace bicarbonate which will be absorbed at the proximal tubule

268

Proximal RTA (Type II)

- decreased ability for kidney to reabsorb most of filtered bicarbonate
- eventually bicarbonate is lost in urine until the body is so depleted of bicarbonate that the distal tubule can absorb the rest
- the urine pH will become low (at or below 5.5)
- chronic metabolic acidosis can leach calcium to cause osteomalacia

269

Proximal RTA (Type II): Causes

- Amyloidosis
- Myeloma
- Fancomi syndrome
- Acetazolamide
- Heavy metal

270

Most accurate test for proximal RTA (Type II)

Testing urine pH after giving bicarbonate

271

Urine pH during proximal RTA (Type II)

First it is basic (above 5.5) until most bicarbonate is lost from body, then is low (below 5.5)

272

Status of potassium in both proximal and distal RTA

Hypokalemia
- potassium is lost in the urine

273

Proximal RTA (Type II)

Thiazide diuretics cause volume depletion. Volume depletion will enhance bicarbonate reabsorption.

274

Hyporeninemia, hypoaldosteronism (Type IV RTA)

- occurs most often in diabetes
- decreased amount or effect of aldosterone at the kidney tubule
- leads to loss of Na and retention and K and H_

275

Best testing for Type IV RTA

Finding a persistently high urine sodium despite a sodium depleted diet

276

Treatment for Type IV RTA

Fludrocortisone
- steroid with the highest mineralcorticoid or "aldosteronelike" effect

277

Urine anion gap (UAG)

way to distinguish between diarrhea and RTA
Na - Cl

278

Why is chloride high in acidotic conditions

Acid excreted by kidney is buffered by NH4Cl
- more acid excreted, the greater amount of chloride found in urine

279

Why is the UAG (Na - Cl) positive in RTA

RTA is defect in acid excretion into urine, so the amount of chloride in urine is diminished

280

Why is UAG (Na - Cl) negative in RTA

diarrhea associated w/ metabolic acidosis thus kidney tries to compensate by increasing acid excretion
- acid is excreted with chloride
- more acid in urine means more chloride in urine

281

Causes of metabolic acidosis

MUDPILES
Methanol
Uremia
Diabetes ketoacidosis
Paraaldehyde
Isoniazid or Iron
Lactate
Ethylene glycol
Salicylates

282

Metabolic acidosis 2/2 lactate

- caused by hypotension or hypoperfusion
- tested with blood lactate levels
- treat by correcting hypoperfusion

283

Metabolic acidosis 2/2 ketoacidosis

- caused by DKA and starvation
- tested by measuring acetone levels
- treat with insulin and fluids

284

Metabolic acidosis 2/2 oxalic acid

- caused by ethylene glycol overdose
- tested by seeing crystals in UA
- treat with fomepizole and dialysis

285

Metabolic acidosis 2/2 formic acid

- caused by methanol overdose
- tested by seeing inflamed retina
- treated with fomepizole and dialysis

286

Metabolic acidosis 2/2 uremia

- caused by renal failure
- test by evaluating BUN and Cr
- treated with dialysis

287

Metabolic acidosis 2/2 salicylates

- caused by aspirin overdose
- test for aspirin levels
- treat by alkanizing urine

288

ABG in metabolic acidosis

- decreased pH below 7.4
- decreased pCO2 indicating respiratory alkalosis as compensation
- decreased bicarbonate

289

Metabolic alkalosis

- elevated serum bicarbonate level
- compensated with respiratory acidosis
- relative HYPOventilation that will increased pCO2 to compensate for metabolic alkalosis

290

Metabolic alkalosis: etiology

- GI loss: vomiting or nasogastric suction
- Increased aldosterone: primary hyperaldosteronism, Cushing syndrome
- Diuretics
- Milk-alkali syndrome: high volume liquid antacids
- Hypokalemia: H+ move into cells so K can be released

291

Metabolic alkalosis on ABG

- increased pH > 7.4
- increased pCO2 indicating respiratory acidosis as compensation
- increased biarbonte

292

Minute ventilation

respiratory rate x tidal volume

293

Respiratory alkalosis

- decreased pCO2
- increased minute ventilation
- metabolic acidosis as compensation

294

Causes of respiratory alkalosis

- Anemia
- Anxiety
- Pain
- Fever
- Interstitial lung disease
- Pulmonary emboli

295

Respiratory acidosis

- increased pCo2
- decreased minute ventilation
- metabolic alkalosis as compensation

296

Respiratory acidosis: causes

- COPD / emphysema
- Drowning
- Opiate overdose
- Alpha 1 antitryspin deficiency
- Kyphoscoliosis
- Sleep apnea / morbid obesity

297

Most common cause of kidney stones (nephrolithiasis)

Calcium oxalate
- which forms more frequently in an alkaline urine

298

Most common risk factor for kidney stones

Overexcretion of calcium in the urine

299

A 46 y/o M comes to the ER with excruciating pain in his left flank radiating to the groin. He has some blood in his urine. What is the most appropriate next step in the management of this patient?

Katerolac
- NSAID
- more important to provide relief than specific diagnostic testing

300

What is the most accurate diagnostic test for nephrolithiasis?

CT scan

301

Why does Crohn disease cause kidney stones?

Increased oxalate absorption

302

Best initial therapy for acute renal colic

- Analgesic and hydration
- CT and sonography to detect obstruction
- Stones < 5 mm pass spontaneously
- Stones 5 - 7 mm get nifedipine and tamsulosin to help them pass

303

Kidney stone etiology is determined with

- Stone analysis
- Serum calcium, NA, uric acid, PTH, Mg, and phosphate levels
- 24 hr urine for volume, Ca, oxalate, citrate, cysteine

304

Uric acid stones

- not detectable on X-ray but seen on CT

305

Cysteine stones

- managed with surgical removal, alkalinizing the urine

306

Woman with her 1st episode of renal colic is found to have a 1.8 cm stone in the L renal pelvis. She has no obstruction and her renal function is normal (normal BUN and Cr) What is the most appropriate next step in teh management of this patient?

Lithotripsy

307

UTIs leave patients prone to which type of kidney stones?

Struvite stones (Mg/Al/ P)

308

Long term management of nephrolithiasis

50% of those with kidneys stones will have reoccurence within 5 years

309

Man with a Ca oxalate stone is managed with lithotripsy and the stone is destroyed and passes. His urinary calcium level is increased. Besides increasing hydration, which will most likely benefit this patient?

Hydrochlorothiazide
- removes calcium from urine

310

Metabolic acidosis and stone formation

Metabolic acidosis removes Ca from bones and increases stone formation
- acidosis decreases citrate levels
- citrate binds calcium making it unavailable for stone formation

311

Urinary Stress incontinence

- older woman w/ painless urinary leakage with coughing, laughing, or lifting heavy objects

312

Best test for urinary stress incontinence

have patient stand and cough
- observe for leakage

313

Urinary stress incontinence: treatment

1. Kegel exercises
2. Local estrogen cream
3. Surgical tightening of urethra

314

Urinary urge incontinence

- sudden pain in the bladder followed immediately by overwhelming urge to urinate

315

Best test for urinary urge incontinence

pressure measurement in half full bladder
manometry

316

Urinary urge incontinence: treatment

1. Bladder training exercises
2. Local anticholinergic therapy
- oxybutinin
- tolterodine
- solifenacin
- dariferancin
3. Surgical tightening of urethra

317

Hypertension

- systolic pressure > 140 mm Hg
- diastolic pressure > 90 mm Hg
- diabetic patient or someone with CRD > 130/80 mm Hg

318

Most common disease in the US

hypertension

319

Most common risk factor for the most common cause of death

Myocardial infarction

320

Causes of hypertension

- Renal artery stenosis
- Glomerulonephritis
- Coarctation of the aorta
- Acromegaly
- Sleep apnea
- Pheochromocytoma
- Hyperaldosteronism
- Cushing syndrome
- Congenital adrenal hyperplasia

321

Hypertension: symptomatic presentation

- CAD
- Cerebrovascular disease
- CHF
- Visual disturbance
- Renal insufficiency
- Peripheral arteru disease

322

Renal artery stenosis: presentation

- HTN
- bruit is auscultated at the flank
- continuous throughout systole and diastole

323

Coaractation of the aorta

- HTN
- upper extremities > lower extremities