renal Flashcards

1
Q

ESRF and contrast

A

When patients are dialysis-dependent it would be potentially dangerous to “pre-hydrate” the patient and potentially fluid overload them. Dialysis-dependent patients who receive contrast for a CT scan may need haemodialysis to remove the contrast. This is particularly important when they have some residual renal function that should be preserved as far as possible (as it makes their fluid balance much easier to manage between dialysis sessions).

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2
Q

ALARM symtoms

A

vomiting
dysphagia
weight loss
bleeding

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3
Q

Bartters syndrome

A

Bartter’s syndrome is a rare, autosomal recessive disorder, caused by one of three mutations of the ion transporter or ion channel present in the thick ascending limb of the distal nephron.

Type I and II mutations present in infancy (often following premature birth and polyhydramnios) with severe dehydration, hypokalaemic alkalosis, hypercalciuria and nephrocalcinosis. Mortality is high.

Type III mutations present with a more varied clinical picture to type I and II, ranging in severity from near fatal volume depletion with hypokalaemic alkalosis and respiratory arrest, to mild disease presenting in teenagers with weakness and polyuria. Nephrocalcinosis has not been described in type III mutations, therefore it can differentiate between type I and II disease, and type III disease.

Management is with long term potassium supplementation and care to avoid dehydration. The long term prognosis is uncertain.

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4
Q

Liddles syndrome

A

Liddle’s syndrome is a congenital form of salt-sensitive hypertension characterised by a very high rate of renal sodium uptake, despite low levels of aldosterone, secondary hypokalaemia and metabolic alkalosis.

It is caused by a congenital mutation, which causes a constitutive hyper-reactivity in the epithelial sodium channel (ENaC). The increased sodium uptake is accompanied by an increased water uptake, leading to an increase in blood volume and secondary hypertension.

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5
Q

nephrotic syndrome complicatins

A

If the nephrotic syndrome is left unchecked, complications include:

streptococcal sepsis
venous thromboembolism, and
hypercholesterolaemia.

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6
Q

prognosis proteinuria

A

Beta-2-microglobulin has been shown to be predictive of risk of progression of disease in myeloma, myelodysplastic syndrome, and chronic myeloid leukaemia.

In myeloma it is an accurate estimate of total disease load, with guidelines suggesting that a beta-2-microglobulin level of >3.5 mg/L is strongly associated with increased mortality and morbidity.

Other prognostic indicators in myeloma include:

Hypercalcaemia
Creatinine
Severity of anaemia
Viscosity
Lactate dehydrogenase level, and
Recurrent bacterial infections.
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7
Q

features of chronic graft v host disease

A

The answer is beta-2 microglobulin.

Beta-2-microglobulin has been shown to be predictive of risk of progression of disease in myeloma, myelodysplastic syndrome, and chronic myeloid leukaemia.

In myeloma it is an accurate estimate of total disease load, with guidelines suggesting that a beta-2-microglobulin level of >3.5 mg/L is strongly associated with increased mortality and morbidity.

Other prognostic indicators in myeloma include:

Hypercalcaemia
Creatinine
Severity of anaemia
Viscosity
Lactate dehydrogenase level, and
Recurrent bacterial infections.
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8
Q

metabollic alkalosis

A

The elevated bicarbonate also indicates a metabolic cause is likely. In longstanding respiratory alkalosis, the bicarbonate may fall in compensation.

Causes of respiratory alkalosis:

Central causes - stroke, meningitis, CNS tumour
Drugs - salicylates
Anxiety
Pregnancy.
Causes of metabolic alkalosis:

Vomiting - anorexia nervosa, gastric outlet obstruction
Ingestion of base
Prolonged hypokalaemia of any cause - the kidney allows H+ to be lost in an effort to retain K+. Diuretic therapy is a common example.
Burns.

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9
Q

phosphate binder

A

. Sevelamer is a non-aluminium containing phosphate binder, and as such is a reasonable option for patients with end stage renal failure with raised serum phosphate levels.

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10
Q

cryoglobulinemia

A

cryoglobulinaemia secondary to chronic hepatitis C infection giving rise to acute kidney injury, mononeuritis multiplex and cutaneous vasculitis.

Membranoproliferative glomerulonephritis (also known as mesangiocapillary glomerulonephritis) is the characteristic histological finding on biopsy where there is renal involvement. It is characterised by mesangial and endothelial cell proliferation, expansion of the mesangial matrix and thickening of the peripheral capillary walls.

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11
Q

Meckels diverticulum

A

Meckel’s diverticulum is the vestigial remnant of the omphalomesenteric duct. It is normally located in the terminal ileum within ~60 cm of the ileocaecal valve and it averages 6 cm in length.

About 50% of these contain ectopic gastric mucosa, commonly leading to clinical presentations of peptic ulceration and haemorrhage.

Other complications of Meckel’s diverticulum include

Diverticulitis
Intussusception
Perforation
Obstruction.
Although it occurs much more commonly in children it is an important differential consideration for gastrointestinal bleed in adults.

Tc-99m pertechnetate accumulates in gastric mucosa and is the study of choice for identifying ectopic gastric mucosa in a Meckel’s diverticulum.

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12
Q

Refeeding syndrome

A

Refeeding syndrome occurs when malnourished individuals are given nutritional support (or simply recommence food intake). Individuals need only to have been starved for as little as five days to be at risk.

Patients may present with symptoms ranging from weakness to alterations in mental state, neurological abnormalities (dysarthria, diplopia) and rhabdomyolysis. The triad of electrolyte abnormalities of hypophosphataemia, hypokalaemia and hypomagnesaemia is characteristic.

Management involves correcting electrolyte abnormalities aggressively and carefully controlling calorific intake. Calorie intake may need to be reduced to less than 50% of the recommended amount.

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13
Q

renal transplant post op comps

A

deterioration in renal function soon after a renal transplant. These include:

Hyperacute rejection (which usually occurs in hours)
Acute tubular necrosis, and
Surgical complications (renal arterial or venous thrombosis and ureteric stenosis).
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14
Q

CKD and anemia

A

The target haemoglobin range is 100-120 g/L and it is recommended that measures to investigate and manage anaemia related to chronic kidney disease should be instigated when the haemoglobin level falls below 110 g/L.

ferritin <100 μg/L should be considered an indicator of absolute iron deficiency.

Transferrin saturation <20% is a marker of functional iron deficiency

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15
Q

amyloidosis

A

Amyloidosis is a common cause of neurological impairment in patients on longstanding dialysis. It is caused by β2 microglobulin accumulation. It causes joint pains and stiffness, usually upper limbs more than lower limbs. The only treatment is renal transplantation. It can be reduced by using high flux dialysis membranes in patients who are likely to be on dialysis for a prolonged period.

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16
Q

uraemia

A

Uraemia may cause neurological symptoms. This is more common in men, and mostly affects the legs.

Sensory symptoms (paraesthesia, burning sensations and pain) occur before motor symptoms (muscle atrophy, myoclonus, paralysis). The sensory symptoms may improve with starting or increasing the frequency of dialysis, but the motor symptoms are not reversible.

17
Q

AIN

A

Acute interstitial nephritis is inflammation of the renal tubulo-interstitium, secondary to a hypersensitivity reaction to drugs. The most common drug related cause is NSAIDs.

Other precipitating drugs include

Antibacterials (penicillins, cephalosporins, sulphonamides, rifampicin)
Loop diuretics (furosemide)
Thiazide diuretics
Amphotericin
Cimetidine
Allopurinol.
Features include acute, most commonly oliguric renal failure, with or without systemic features which include fever, arthralgia and skin rashes. Many patients have eosinophilia, raised serum IgE and eosinophiluria.

Renal biopsy shows oedema of the interstitum with infiltration of plasma cells, lymphocytes and eosinophils, with acute tubular necrosis and variable tubular dilatation.

The treatment includes withdrawal of the offending drug, and may involve dialysis until normal renal function returns.

18
Q

complication hypernephroma

A

polycythaemia is a well recognised complication of hypernephroma due to erythropoietin secretion.

Others include:

Canon ball metastatses
Hypertension
Hypercalcaemia.

19
Q

IgA nephropathy

A

Mesangial widening, inflammation and mesangial cell proliferation are common features on renal biopsy in IgA nephropathy. Granular IgA deposits on immunofluorescence are the hallmark of the disease and give it its name.

20
Q

Rapid diffuse GN

A

Crescentic changes are more often associated with ANCA positive vasculitides or anti-GBM disease.

21
Q

minimal change biopsy

A

Diffuse membrane thickening is found in membranous glomerulonephritis, podocyte fusion in minimal change disease

22
Q

management of renal artery stenosis

A

unilateral renal artery stenosis (RAS), and this is the most likely cause for his hypertension. The current evidence favours medical therapy in these patients, that is, an antiplatelet agent (aspirin), lipid lowering therapy (simvastatin) and tight blood pressure control (amlodipine).

23
Q

indications for RRT

A

The initiation of emergency renal replacement therapy is usually required for:

Acute life threatening hyperkalaemia which is resistant to treatment. In this example the potassium is within normal limits.
Development of metabolic acidosis which is non-responsive to fluid. In this instance the pH is within normal limits.
Development of fluid overload, which may manifest itself as pulmonary oedema.
Development of uraemia which may manifest itself as pericarditis (not pancreatitis), neuropathy and confusional state.

24
Q

BP and CKD

A

patients with chronic kidney disease who have proteinuria equivalent to ACR ≥70 mg/mmol should have their blood pressure controlled to the target range 120-129/<80 mmHg.

120-139/<90 mmHg should be used in non-diabetic patients with chronic kidney disease and an ACR <70 mg/mmol.

25
Q

ATN

A

ATN is a cause of intrarenal AKI, severe ischemia leading to the death of tubular cells.

In acute tubular necrosis (ATN), urine to plasma osmolality should be less than 1.1, urinary sodium excretion is typically more than 60 mmol/L and urinary urea excretion less than 160 mmol/L. Brown granular casts

If this patient had a physiological oliguria, there would still be preservation of urine concentration, with low urinary sodium. Prerenal uraemia - kidneys hold on to sodium to preserve volume

Both ATN and pre-renal failure can present with a fall in urine output. There is such a marked variation in urine urea concentration, that it is seldom used as a clinical guide.

causes: NSAIDS, gent

26
Q

optimising iron in CKD

A

In order to maximise the efficacy of erythropoietin in the treatment of the anaemia of chronic kidney disease it is important to make sure that patients’ iron statuses are adequately optimised. This is defined as maintaining the ferritin >200 μg/L and transferrin saturation >20%. Where oral supplementation is insufficient intravenous iron therapy is required.

27
Q

SLE nephrtis

A
I - minimal mesangial - nephritic
II - mesangial proliferative - nephritic
III - focal - nephrotic
IV - diffuse - most common and severe. nephrotic, IgG deposits throughout
V - membranous - nephrotic
VI - advanced sclerosis

Cyclophosphamide, mycophenolate mofetil and azathioprine reduce mortality in proliferative forms of lupus glomerulonephritis. Immunosuppressive therapy is required in these cases to prevent progressive to end-stage renal failure.

28
Q

RTA

A

RTA: metabolic acidosis, hyperhcloremia, normal anion gap

type 1 (distal): defect results in H+ resorption. metabolic acidosis, hyperchloremia, hypokalemia. hypocalcemia, reduced vitamin D uptake = osteomalacia and calcium phosphate stones

type 2 (proximal): defect results in HCO2- excretion.

type 3 = 1 & 2

type 4: fanconi sydrome excretion of glucose, amino acids, phosphate in urine. hypercalemia

29
Q

bartter’s and giettlemans

A

hypokalemia, metabollic alkalosis

bartters: salt-wasting. hypokalemia, alkalosis, like loop diureitic = hypercalciuria

giettlemans = hypokalemia, metabolic alkalosis, hypocalciuria like thiazide diuretic