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4th year everything > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Water and electrolytes are taken in by food and water and lost in urine and sweat. What other, insensible water losses are there?

A

500ml lost by expiration per day

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2
Q

What percentage of an adult’s body weight is water?

A

50-60%

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3
Q

In the healthy 70kg male, total body water is approx. how many litres?

A

42L

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4
Q

What are the three major body fluid compartments?

A

Intracellular, extracellular and plasma

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5
Q

Which is the largest of the body fluid compartments?

A

Intracellular

Approx. 28L (35% of lean body weight)

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6
Q

Describe the extracellular fluid compartment

A

The extracellular fluid compartment comprises of the interstitial fluid that bathes the cells (9.4L/12% of body weight)

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7
Q

What is osmotic pressure?

A

The primary determinant of the distribution of water among the three major compartments

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8
Q

What is osmolality?

A

Defined as the number of osmoles per KILOGRAM of solution

Measurement of the osmotic concentration

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9
Q

What is osmolarity?

A

Defined as the number of osmoles per LITRE of solution

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10
Q

What electrolyte predominates in the intracellular compartment?

A

Potassium

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11
Q

What electrolytes predominates in the interstitial fluid?

A

Sodium salts

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12
Q

What molecules determine the oncotic pressure within the plasma?

A

Proteins

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13
Q

What are the daily water requirements?

A

25-30ml/kg/day

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14
Q

What are the daily requirements for sodium, potassium and chloride?

A

1mmol/kg/day

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15
Q

What are the daily requirements for glucose?

A

50-100 grams/day

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16
Q

What two forces balance to maintain plasma within the vasculature?

A

Hydrostatic pressure (forcing plasma into the interstitium)

Oncotic pressure (pressure exerted by plasma proteins to retain fluid in the vasculature)

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17
Q

What is the definition of oedema?

A

Increase in the interstitial fluids due to one of a number of different aetiologies

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18
Q

Outline some causes of oedema

A

Increased hydrostatic pressure e.g. sodium and water retention in cardiac failure

Reduced oncotic pressure e.g. as a result of nephrotic syndrome with hypoalbuminaemia

Obstruction to lymphatic flow

Increased permeability of the blood vessel wall e.g. local inflammation

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19
Q

What are crystalloids?

A

Sodium chloride 0.9% containing low molecular weight salts or sugars that dissolve completely in water and pass freely between intravascular and interstitial compartments

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20
Q

What are colloids?

A

E.g. dextran 70, gelatin

Contain larger molecular substances and remain for a longer period in the intravascular space than crystalloids

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21
Q

What are colloids used for?

A

Used to expand circulating volume in haemorrhage, burns and sometimes septicaemia

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22
Q

What side effects may accompany administration of colloids?

A

Hypersensitivity reactions including anaphylaxis and a transient increase in bleeding time

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23
Q

What clinical observations may indicate a patient is ‘dry’ (hypovolaemic)?

A

Skin turgor, capillary refill, jugular venous pressure, pulse, lying and standing blood pressure

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24
Q

Why should urine output not be considered alone in the assessment of fluid balance post-operatively?

A

Post-operatively there is a physiological oliguria and an impaired ability of the kidneys to dilute urine; increasing the risk of dilutional hyponatraemia

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25
Q

Before the prescription of IV fluids, clinical assessment of what needs to be undertaken?

A

Establish fluid and electrolyte needs

Identify the type of fluid needed

Does the patient need resuscitation, maintenance etc

Work out the appropriate rate of administration

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26
Q

Regulation of the extracellular volume is determined by the tight control of what electrolyte in particular?

A

Sodium

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27
Q

What is the effective arterial blood volume (EABV)?

A

The fullness of the vasculature; determines the control of renal sodium and water excretion

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28
Q

What two types of volume receptors detect changes in the effective arterial blood volume?

A

Extrarenal: in the large vessels near the heart
Intrarenal: in the afferent renal arteriole

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29
Q

Intrarenal volume receptors have direct control over what hormonal system?

A

The renin-angiotensin-aldosterone system (RAAS)

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30
Q

What hormones counteract the effects of the renin-angiotensin-aldosterone system?

A

Atrial natriuretic peptide - increases sodium excretion

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31
Q

Increased extracellular volume is a result of increased sodium retention/impaired excretion by the kidneys. Outline the symptoms.

A

Interstitial volume overload - ankle oedema, pulomary oedema, pleural effusion and ascites

Intravascular volume overload - raised JVP, cardiomegaly and a raised arterial pressure

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32
Q

List some aetiologies of extracellular volume expansion

A

Cardiac failure
Cirrhosis
Nephrotic syndrome
Sodium retention

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33
Q

How does cirrhosis lead to extracellular volume expansion?

A

Complex pathophysiology leading to vasodilation and under perfusion of the volume receptors.

Hypoalbuminaemia may contribute

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34
Q

List some common causes of decreased extracellular volume?

A

Haemorrhage
Plasma loss in burns
Pathological diuresis

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35
Q

Signs of volume depletion may occur in a patient with a normal volume. Give an example of when this occurs?

A

Sepsis (due to vasodilation and increased capillary wall permeability)

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36
Q

What is the most potent class of diuretics? Give an example

A

Loop diuretics e.g. furosemide

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37
Q

What is the mechanism of action of loop diuretics?

A

Reduce Na+/Cl- reabsorption from the ascending loop of Henle in the glomeruli

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38
Q

What is the mechanism of action of thiazide diuretics? Give an example

A

Reduced Na+ reabsorption at the distal convoluted tubule of the glomeruli

Bendroflumethiazide

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39
Q

Spironolactone is an example of what class of diuretics?

A

Aldosterone antagonists

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40
Q

Give an example of a potassium-sparing diuretic

A

Amiloride

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41
Q

Give common signs and symptoms of volume depletion

A

Symptoms - thirst, nausea, dizziness (postural)

Signs - loss of skin tugor, peripheral vasoconstriction, tachycardia, low JVP, postural hypotension

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42
Q

What are the dangers of severe volume depletion?

A

Impaired cerebral perfusion leading to confusion and eventual coma

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43
Q

What device allows the measurement of the central venous pressure?

A

Central venous line

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44
Q

If the kidneys are working well, what is the expected normal value of urinary sodium?

A

<20mmol/L

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45
Q

How is circulating volume depletion treated?

Outline the specific treatments for haemorrhage, loss of plasma, loss of sodium/water and loss of water alone

A

Overall principle: Replace what is lost.

Haemorrhage - initial treatment with crystalloid/colloid until packed red cells are available

Loss of plasma (burns/peritonitis) - replace with human plasma/colloid

Loss of sodium and water (vomiting/diarrhoea) - saline or glucose electrolyte solutions

Loss of water - water w. 5% glucose solution to avoid osmotic lysis of red cells

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46
Q

What is the normal value for plasma osmolality?

A

285-300 mosmol/kg

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47
Q

What receptors sense changes in plasma osmolality? Where are they located?

A

Osmoreceptors in the hypothalamus

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48
Q

What mechanisms does the hypothalamus activate on detection of a raised osmolality?

A

Thirst mechanism and release of anti-diuretic hormone (ADH)

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49
Q

What is the action of anti-diuretic hormone?

A

Increases renal reabsorption of water from the collecting ducts

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50
Q

What non-osmotic stimuli may also cause secretion of ADH?

A

Hypovolaemia
Stress (surgery/trauma)
Nausea

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51
Q

What is the other name for the hormone ADH?

A

Vasopressin

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52
Q

What physiological phenomena occurs at a plasma osmolality of less than 275 mosmol/kg?

A

Complete suppression of ADH secretion

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53
Q

What is the definition of hyponatraemia?

A

Reflects too much water in relation to sodium.

Serum sodium < 135 mmol/L

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54
Q

List four aetiologies of hyponatraemia

A
  1. Water excess (dilutional hyponatraemia)
  2. Salt loss e.g. diarrhoea
  3. Pseudohyponatraeia (hyperlipidaemia causing spuriously low sodium - no treatment required)
  4. Artefactual hyponatraemia - blood sample taken from an arm where a low sodium drip is being infused e.g. glucose
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55
Q

What is the essential distinction a clinician must make when assessing the hyponatraemia patient?

A

Is the patient either:

Hypovolaemia
Euvolaemic
Hypervolaemic

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56
Q

How is hypovolaemic hyponatraemia treated?

A

Restoration of extracellular volume crystalloids or colloids normalises serum sodium

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57
Q

What is the most common cause of hypovolaemia hyponatraemia?

A

Diuretics over-use

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58
Q

What is the most common cause of dilutional hyponatraemia (hypovolaemic)?

A

Overuse of 5% glucose in post-operative patients

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59
Q

What three pathologies often precipitate dilutional hyponatraemia?

A

Severe cardiac failure, cirrhosis, nephrotic syndrome

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60
Q

What are the consequences of not correcting dilutional hyponatraemia?

A

Due to the movement of water into brain cells (cerebral oedema)

Headache, confusion, convulsions and coma

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61
Q

How is dilutional hyponatraemia managed?

A

Most cases managed by water restriction

Review of diuretic treatment may be indicated

Vasopressin V2 receptor antagonists e.g. tolvaptan produces free water diuresis

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62
Q

What is central pontine myelinolysis?

A

Over-rapid correction of sodium concentration leading to severe neurological damage causing quadriparesis, respiratory arrest, pseudobulbar palsy, mutism, seizure

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63
Q

What is the most common cause of hypernatraemia?

A

Reduced water intake or water loss in excess of sodium

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64
Q

What are the clinical features of hypernatraemia?

A

Nausea, vomiting, confusion

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65
Q

Serum levels of potassium are regulated by what three factors?

A
  1. Uptake of K+ into cells
  2. Renal excretion - mainly controlled by aldosterone
  3. Extrarenal losses e.g. gastrointestinal
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66
Q

What is the definition of hypokalaemia?

A

Serum potassium concentration of <3.5 mmol/L

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67
Q

What are the most common causes of hypokalaemia?

A

Diuretic treatment

Hyperaldosteronism

68
Q

What are the clinical features of hypokalaemia?

A

Usually asymptomatic

Muscle weakness and cardiac arrhythmias if severe

69
Q

How is hypokalaemia managed?

A

Assessment of diuretic treatment

Replacement with oral potassium chloride

70
Q

What other electrolyte must be normalised before hypokalaemia can be normalised?

A

Magnesium

Hypomagnesaemia makes hypokalaemia difficult/impossible to correct

71
Q

Under what circumstances may IV potassium be indicated?

A

Severe hypokalaemia associated with cardiac arrhythmias and hypokalaemia diabetic ketoacidosis

72
Q

What is the definition of hyperkalaemia?

A

> 5mmol/L

73
Q

What are the most common causes of hyperkalaemia?

A 
Renal impairment (e.g. AKI)
Diabetic ketoacidosis 
Addison's disease
74
Q

What are the clinical features of hyperkalaemia?

A

Produces few symptoms until it causes cardiac arrest

Causes progressive ECG changes

75
Q

How is mild hyperkalaemia managed?

A

Mild disturbance causes dietary potassium restriction

76
Q

What ECG changes may be seen in hyperkalaemia?

A

Reduced P wave
Wide QRS complex
Tented T waves
‘Sine wave’ pattern

77
Q

How is severe hyperkalaemia treated?

A

Protection of myocardium - 10ml of 10% calcium gluconate

Drive K+ into cells - Soluble 10 units of insulin and 50ml of 50% dextrose

Deplete body K+ - polystyrene sulphonate resin orally

78
Q

What are the two effects magnesium has on potassium and PTH?

A

Increases renal excretion of potassium

Leads to parathyroid hormone resistance

79
Q

What is the management of hypomagnesaemia?

A

Underlying causes must be corrected

Oral supplements in mild disease

IV supplementation in severe disease (plus loading dose)

80
Q

What is the most common cause of hypermagnesaemia?

A

Usually iatrogenic in patients with renal failure who have been given magnesium-containing antacids/laxatives

81
Q

What are the clinical features of hypermagnesaemia?

A

Neurological,respiratory and cardiovascular depression

82
Q

How is hypermagnesaemia treated?

A

Mild - stopping magnesium-containing drugs

Severe - IV calcium gluconate with dextrose/insulin to lower plasma magnesium

83
Q

What is the normal range of pH?

A

7.35-7.45

84
Q

What molecule is the main plasma and extracellular fluid buffer?

A

Bicarbonate

85
Q

Where is bicarbonate excreted and reabsorbed respectively?

A

Filtered out at the glomerulus and reabsorbed at the proximal and distal renal tubules

86
Q

What enzyme facilitates the bicarbonate equilibrium?

A

Carbonic anhydrase

87
Q

What compensatory mechanism is triggered by metabolic acidosis? What receptors detect and trigger this?

A

Hyperventilation

Via medullary chemoreceptors

88
Q

What compensatory mechanism is triggered by respiratory acidosis?

A

Renal bicarbonate retention

89
Q

The measurement of what three things reveal the nature of an acid/base disturbance? What clinical procedure does this describe?

A

pH
PaCO2
[HCO3-]

All measured in an arterial blood gas sample

90
Q

What is metabolic acidosis? What is the most common cause?

A

Accumulation of any acid other than carbonic acid.

Most commonly lactic acidosis following shock or cardiac arrest

91
Q

What are the clinical features of metabolic acidosis?

A

Hyperventilation, hypotension and cerebral dysfunction (fits and confusion)

92
Q

What is the first step in the differential diagnosis of metabolic acidosis?

A

Measure the anion gap.

Essentially tells you whether the acidosis is due to retention of HCl or another acid.

93
Q

What are the most common causes of metabolic acidosis with a normal anion gap?
(ABCD)

A

Addison’s
Bicarbonate loss e.g. diarrhoea or renal tubular damage
Chloride
Drugs- acetazolamide

94
Q

What are the most common causes of metabolic acidosis with an increased anion gap?

A 
Lactic acidosis (sepsis)
Uraemic acidosis
Diabetic ketoacidosis
Alcohol
Acid poisoning (methanol, Salicylates)
95
Q

Outline lactic acidosis

A

Occurs when cellular respiration is anaerobic (type A) or due to metabolic abnormality (type B).

Type A occurs in septicaemia and cardiogenic shock

96
Q

Outline diabetic ketoacidosis

A

Accumulation of acetoacetic and hydroxybutyric acids

97
Q

Outline renal tubular acidosis

A

Failure of the kidney to acidify urine properly

98
Q

Outline uraemic acidosis

A

Reduction of the capacity to secrete H+ and NH4+.

Associated with hypercalcaemia and renal osteodystrophy

99
Q

Metabolic alkalosis is most often associated with what two pathologies?

A
  1. Volume depletion

2. Potassium depletion

100
Q

What are the main causes of metabolic alkalosis?

A

Persistent vomiting, diuretic therapy or hyperaldosteronism

101
Q

What is one of the earliest signs of alkalosis?

A

Cerebral dysfunction

102
Q

How is metabolic alkalosis managed?

A

Fluid replacement

103
Q

What is the functional unit of the kidney?

A

Nephron

104
Q

What structure regulates elimination of potassium and non-volatile hydrogen ions?

A

Distal tubules

105
Q

What are the two most common diseases of the kidney or urinary tract in men and women respectively?

A

Men - BPH

Women - UTI

106
Q

List some symptoms indicative of renal tract disease?

A

Dysuria, frequency of micturition, haematuria, urinary retention, alteration of urine volume (oliguria, polyuria)

107
Q

What may be the presenting symptoms/incidental findings of chronic kidney disease?

A

Lethargy, anorexia, pruritis

Incidental finding of hypertension, raised serum urea, proteinuria/ haematuria

108
Q

What are the vasa recta?

A

Vessels supplying the loop of Henle

109
Q

List the causes of dysuria

A
  1. Inflammation of urethra (urethritis) or bladder (cystitis)
  2. Inflammaiton of the vagina/glans by candida albicans or gardnerella vaginalis
110
Q

Outline management of the oliguric patient

A
  1. Exclude obstruction - due to acute retention (great discomfort, dull blader to percussion)
  2. Assess for hypovolaemia (BP, pulse, JVP, urinary electrolytes)
  3. Management of established AKI (diagnosed after 1. and 2. have been ruled out)
111
Q

Outline some causes of loin/flank pain

A

Acute pyelonephritis
Upper urinary tract obstruction
Occlusion of the renal artery
Thrombosis/emboli

112
Q

How is renal function assessed?

A

Estimation of glomerular filtration rate (eGFR)

113
Q

What equation is used to calculate eGFR from serum creatinine?

A

Cockrof-Gault equation

114
Q

Outline what is possible to test for with urinary dipstick testing

A

Blood, protein, glucose, ketones, bilirubin, urobilinogen, pH, nitrates, leukocytes

115
Q

What is considered to be normal urinary protein excretion?

A

<150mg/day

116
Q

What is the nephrotic range of proteinuria?

A

> 3.5g per day (PCR >350mg/mm)

117
Q

What is microalbuminuria?

A

Increase above the normal range of urinary albumin excretion that is undetectable by conventional dipsitcks

118
Q

What is the clinical usefulness of testing for microalbuminuria?

A

Predictor in the development of diabetic nephropathy

119
Q

How is microalbuminuria measured?

A

Albumin/creatinine ratio (ACR) >2.5mg/mmol in men and >3.5mg/mmol in women

120
Q

Haematuria can arise from several sites. Outline how the bleeding pattern can indicate different sites

A

Blood at the beginning of micturition - urethral disease

Blood at the end of micturition - bladder/prostate disease

Blood seen as even discolouration - bleeding above the bladder (e.g. ureters/kidneys)

121
Q

List some transient causes of haematuria

A

UTI

Contamination of urine from menstruation

122
Q

List some imaging techniques of renal pathology

A 
Plain X-ray 
US
MRI
Excretion Urography (IVU)
Renal angiography 
Anterograde pyelography (outlines 
Retrograde pyelography
Renal scintigraphy
123
Q

What is the difference between glomerulonephritis and glomerulopathy?

A

On microscopic examination of renal biopsies, if inflammation is predominant, it can be described as glomerulonephritis. Otherwise, it is glomerulopathy

124
Q

In term of renal disease description, what is meant by the term ‘focal’?

A

Some, but not all of the glomeruli are affected

125
Q

In term of renal disease description, what is meant by the term ‘diffuse’?

A

Approx. >75% of glomeruli contain the lesion

126
Q

In term of renal disease description, what is meant by the term ‘segmental’?

A

Only a part of the glomerulus is affecte

127
Q

In term of renal disease description, what is meant by the term ‘global’?

A

All glomeruli involved

128
Q

In term of renal disease description, what is meant by the term ‘proliferative’?

A

An increase in cell numbers due to hyperplasia of one or more of the resident glomerular cells

129
Q

In term of renal disease description, what is meant by the term ‘membrane alterations’?

A

Capillary wall thickening due to deposition of immune complexes in the basement membrane

130
Q

In term of renal disease description, what is meant by the term ‘crescentic’?

A

Epithelial cell proliferation with mononuclear infiltration in Bowmann’s space

131
Q

What is the typical history of a person with glomerular disease?

A

Suspected in patients presenting with haematuria, red cell casts and proteinuria

132
Q

Glomerular disease can be classified into four main syndromes; what are they?

A
  1. Nephrotic syndrome
  2. Acute glomerulonephritis (acute nephritic syndrome)
  3. Rapidly progressive glomerulonephritis
  4. Asymptomatic haematuria/ proteinuria (or both)
133
Q

What is nephrotic syndrome?

A

Massively increased filtration fo macromolecules resulting in:

  1. Hypoalbuminaemia - a consequence of massive proteinuria
  2. Oedema (due to sodium retention in renal collecting tubules)
  3. Hypercholesterolaemia (due to increased synthesis)
134
Q

What is the difference between active and bland sediments?

A

Sediments are precipitates in your urine. Active sediments have cellular components e.g. RBCs, WBCs, casts - usually indicate an active process of renal damage

Bland sediments are proteins, crystals or casts

135
Q

What are the differential diagnoses for a patient with nephrotic syndrome and bland urinary sediments?

A

Membranous nephropathy and focal segmental glomerulosclerosis in adults

Minimal-change nephropathy in children

136
Q

What is membranous nephropathy?

A

Deposition of IgG and C3 in the basement membrane attributed to a number of causes including drugs (e.g. NSAIDs, penicillamine etc.), autoimmune processes (e.g. SLE), malignancy, infections (hepatitis B/C, schistosomiasis)

137
Q

What is focal segmental glomerulosclerosis?

A

A particularly common cause of nephrotic syndrome in black adults. Similar histological types in HIV infection

138
Q

What is minimal change nephropathy?

A

Accounts for over 90% of nephrotic syndrome in children.

Unknown pathogenesis with no immunofluorescent immune complexes.

Glomeruli appear normal on light microscopy

139
Q

Outline some non-immune mediated causes of nephrotic syndrome

A

Renal amyloid and diabetes mellitus

140
Q

What are the differential diagnoses for a patient with nephrotic syndrome and active urinary sediments?

A

Mesangiocapillary (membranoproliferazive glomerulonephritis)
Mesangial Proliferative Glomerulonephritis

141
Q

What is Mesangiocapillary (membranoproliferazive glomerulonephritis)?

A

Occurs with chronic infection (e.g. abscesses, infective endocarditis, hepatitis C) and leads to progressive renal failure

142
Q

What is Mesangial Proliferative Glomerulonephritis?

A

Heavy proteinuria with minimal changes on microscopy. Glomerular mesangium deposition of IgM and/or complement

143
Q

What are the clinical features of nephrotic syndrome?

A

Oedema of the ankles, genitals, abdominal wall

144
Q

What are the differential diagnoses for nephrotic syndrome?

A

Other causes of oedema and hypoalbuminaemia e.g. heart failure, cirrhosis

145
Q

How is nephrotic syndrome managed?

A

General oedema - salt restriction, thiazide diuretic e.g. bendroflumethiazide (followed by furosemide and amiloride in unresponsive patients)

Proteinuria reduced by ACEIs

Specific treatment - minimal change is always steroid-responsive in children

146
Q

What baseline investigations are indicated in glomerular disease?

A

eGFR, urinary protein, serum ureas and electrolytes, serum albumin

147
Q

What are some diagnostically useful tests in glomerular disease?

A

Urine microscopy (to look for red cell casts)
Throat/skin swab culture (for recent strep. infection)
Serum antistreptolysin-O titre (for recent strep. infection)

148
Q

List three complications of glomerular disease (or its treatment) which may occur:

A
  1. Venous thrombosis (renal pain, haematuria, decreasing kidney function - Dx by US)
  2. Sepsis (due to loss of immunoglobulins)
  3. AKI (usually consequence of diuretic therapy)
149
Q

What is acute glomerulonephritis?

A

Often caused by an immune response triggered by an infection or other diseases.

Typically a post-streptococcal GN develops 1-3wks after infection (pharyngitis/cellulitis) with a group A beta-haemolytic strep. bacteria

150
Q

What are the clinical features of acute GN?

A 
Haematuria (visible or non-visible)
Proteinuria 
Hypetension and oedema
Oliguria
Uraemia
151
Q

What diseases are associated with acute GN?

A

Post-infective GN (strep. or others including staph, malaria etc.)

SLE

Infective endocaritis

Henloch-Schönlein Purpura

152
Q

How is acute GN managed?

A

Hypertension treated with salt restriction, loop diuretics and vasodilators

Fluid balance monitored (fluid restriction may be necessary if oedematous)

153
Q

What are the three main causes of rapidly progressive glomerulonephritis?

A
  1. On a background of acute nephritic syndrome
  2. ANti-glomerular basement membrane disease (lung involvement = Goodpasture’s syndrome)
  3. Antibeutrophilic cytoplasmic antibody (ANCA)-associated antibodies
154
Q

List some causative organisms for UTIs

A

E. coli
Proteus mirabilis
Klebsiella aerogenes
Enterococcus faecalis

155
Q

What is meant by the term ‘uncomplicated UTI’?

A

UTI in the otherwise healthy, non-pregnant woman with a functionally normal urinary tract

156
Q

What is urethral syndrome?

A

Occurs in women and presents with dysuria and frequency but in the absence of bacteriuria

May be associated with vaginitis in post-menopausal women, irritant chemicals (e.g. soaps) and sexual intercourse

157
Q

What is bacterial prostatitis?

A

A relapsing infection which presents as perineal pain, recurrent epididymo-orchitis and prostatic tenderness, with pus in expressed prostatic secretion

158
Q

How is bacterial prostatitis treated?

A

Treatment is for 4-6 weeks with drugs that penetrate into the prostate, such as trimethoprim or ciprofloxacin.

159
Q

What are the complications associated with bacterial prostatitis?

A

Prostadynia (prostatic pain in the absence of active infection)

160
Q

What is tubulointerstitial nephritis?

A

Primary injury to the renal tubules and interstitium that results in decreased renal function.

Both acute and chronic

161
Q

Describe acute tubulointerstitial nephritis

A

Mostly due to drug allergy (e.g. NSAIDs, penicillins)

Patients present with fever, eosinophilia and eosinophiluria. proteinuria

Renal biopsy show intense interstitial cellular infiltrate and variable necrosis

Treated by removing the offending drug and high dose prednisolone

162
Q

What is chronic tubulointerstitial nephritis?

A

Many causes including prolonged consumption of large doses of analgesics (particularly NSAIDs)

Presentation is with polydipsia, polyuria and uraemia

163
Q

What are the two main mechanisms by which hypertension complicated bilateral renal disease?

A
  1. Activation of the renin-angiotensin-aldosterone system

2. Retention of salt and water

164
Q

How does renal vascular disease increase blood pressure?

A

Renal perfusion pressure is reduced and renal ischaemia results in increased renin production and blood pressure

165
Q

How is renal artery stenosis investigated and managed?

A

Renal arteriography

Treated with transluminal angioplasty and stent placement

166
Q

What is nephrocalcinosis?

A

Diffuse renal parenchymal calcification that is detectable radiologically

Sx: Painless, hypertension and renal impairment

167
Q

List some causes of nephrocalcinosis

A

Hypercalcaemia
Renal tubular acidosis
Tuberculosis

4th year everything (43 decks)

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