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Renal Flashcards

0
Q

Heavy proteinuria is a sign of what type of disease?

A

Heavy proteinuria is a sign of glomerular disease

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1
Q

What is the normal protein excretion per day?

A

Normal is less than 150mg per day

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2
Q

What is the difference between renal pain and renal colic?
What are the causes of renal pain?
What are the causes of renal colic?

A 
Renal pain is dull constant and in the loin. Renal colic is waxing and waning and radiates to the groin or thigh with vomiting or fever. 
Renal pain is due to:
-pyelonephritis
-renal obstruction
- renal infarction
- acute nephritic syndrome
- poly cystic kidneys

Renal colic may be due to a stone or clot

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3
Q

What is oligouria?

A

Less than 400mL per day for adults or less than 0.5mL/kg/hr

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4
Q

What are the causes of oligouria?

A

Low renal diffusion (dehydration, shock)
Renal parenchymal disease
Renal tract obstruction

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5
Q

What arethecausesof polyuria.

A 
Diabetes mellitus
Diabetes insipid
Hypercalceamia
SVT
Renal medulla disorders (the urine concentration is impaired)
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6
Q

What is acute renal failure?

A

Acute renal failure is the significant decline in renal function over hours to days. ARF is detected by rising creatinine plus or minus oligouria. ARF occurs secondarily to circulatory dysfunction such as hypotension, hypovoleamia, sepsis. It is rarely caused by pri,ary renal disease.

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7
Q

What is chronic kidney disease?

A

Irreversible substantial and long standing loss of renal function also known as chronic kidney disease. CKD is classified according to GFR. There is a poor association between symptoms and severity. Symptoms are likely to be subtle and may be hidden by old age.

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8
Q

What are the two major categories of heamaturia?

A

Heamaturia may be macroscopic or microscopic. Visible or found on dipstick or high powered field microscopic evaluation.

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9
Q

What are the causes of heamaturia?

A

Renal: neoplasia, GN IgAnephropathy, poly cystic kidney,pyelonephritis, trauma
Post renal: calculi, neoplasia, infection, trauma ie from catheter.

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10
Q

What are the causes of proteinuria?

A

Nephrotic syndrome (glomerular or tubular disease), DM, amyloid oasis, Hypertension, interstitial nephritis, heavy metals, multiple ,yelp,a (though dipsticks don’t detect light chains), pregnancy, CCF

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11
Q

What Are the indications of a kidney biopsy?

A

Investigating the cause of acute kidney disease
Investigating glomeruli nephritis eg is persistent heamaturia from IgA nephropathy
To determine the cause of heavy proteinuria after diabetes is excluded
Determine the cause of renal function posttransplantation; rejection, acute tubular necrosis drug toxicity, recurrence of renal disease

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12
Q

What is a UTI? What are the types? What are the risk factors?
What is the main organism?

A

The presence of a pure growth of >10^5 organisms per mL of fresh MSU. Urethritis - in urethra, cystitis -in bladder, Prostitis - in prostate, or pyelonephritis in the renal pelvis.
Risk factors:sex, pregnancy, female, DM, obstruction, catheter, malformation.
The main organism is e.coli.

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13
Q

What are the symptoms of urethritis?
What are the symptoms of pyelonephritis?
How do you treat UTI?

A

Urethritis : dysuria, urgency, heamaturia , supra public pain, foul smelling ursine
Pyelonephritis: flu like symptoms, hugh fevers and vomiting, rigors, low backache, loin pain and tenderness, oligouria if renal failure.
Drink lots of water and take trimethoprim

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14
Q

What are the different types of renal calculi (nephrolithiasis)?

A

Calcium oxalate 75%
Magnesium aluminium phosphate 10-20%
Urate 5%
Hydroxyappetite 5%

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15
Q

What are the tests and findings that you would use or consider for a patient presenting with symptoms of a UTI?

A

Dipstick showing increased nitrites and leukocyte a.
A urine microscopy identifying bacteria and sensitivity, WBCs and possible RBCs.
A culture could also be done, and it might be worth considering a renal ultrasound or as renal abdominal X-ray if there are persistent and severe symptoms that do not respond to conventional treatment. This could show renal abcess, hydro nephrotic, or a calculi.

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16
Q

What is glomerular nephritis?

A

Glomerular nephritis refers to damage to the glomerulus. It consists of a number of diseases that are mostly characterised by inflammatory damage to the glomerulus. Most of these diseases are autoimmune.

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17
Q

What are the key signs and symptoms n glomerulonephritis?

A

Heamaturia (normally microscopic), proteinuria, oedema (if associated with nephrotic syndrome),hypertension (associated with reduced GFR and retention of salts), malaise, nausea, loss of appetite, oligouria, joint pain.
Associated with risk factors: groupA Beta haemolytic streptococcus, hep B, hepC, HIV, SLE, hodgekins lymphoma, haemolytic ureamic syndrome

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18
Q

What are the tests you would order for someone with suspected glomerular nephritis and what results would you be looking for?

A

EUC: elevated creatinine, LFTs: abnormal with hepatitis, low serum albumin, FBC: normochromic, normochromic aneamia, GFR: normal or reduced, 24 hour urine collection: protein<3.5 normally, ultrasound of kidneys:normal or small in chronic disease,
Urinanalysis: dysmorhphic RBCs, heamaturia, proteinuria, WBCs, RBC casts

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19
Q

What treatment is used for glomerulonephritis?

A

Mild disease: treat cause eg. Withdraw drug or give antibx
Moderate disease : control BP with ace inhibitors or ARBs, give fruso IDE if necessary.
Severe disease: give prednisolone. Consider plasmapheresis or immunosuppresants

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20
Q

What are the pathological changes seen in nephritic syndrome? What is the clinical presentation of nephritic syndrome? What are the types of glomerulonephritis that commonly cause nephritic syndrome?

A

Nephritic Syndrome is a type of glomerulonephritis that is caused by inflammation, reactive cell proliferation, breaks in the glomerular basement membrane, and crescent formation. Patients present with heamaturia, RBC casts, dysmorhphic RBCs, proteinuria, htn,and progressive oligouria and renal impairment.
Types of glomerulonephritis that typically present with Nephritic syndrome include IgA nephropathy, anti GBM disease, small vessel vasculitis, and post streptococcal vasculitis.

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21
Q

If someone has oedema, what test should you perform?

A

If someone has oedema, you should always do a dipstick test on a MSU sample in order to avoid missing a potentially serious diagnosis of Nephrotic syndrome.

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22
Q

Which syndrome (nephrotic or nephrotic)of glomerulonephritis is SLE associated with? Which is Minimal change Nephropathy? associated with? Which is diabetic nephropathy? IgA nepropathy? Mesangiocapillaryglomerulonephritis/ membranoproliferative glomerulonephritis ?

A 
SLE -both
IgA -nephritic
Minimal change - nephrotic
Diabetic- nephrotic
MCGN- nephritic, but kind of in the middle
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23
Q

What are the pathological changes seen in Nephrotic syndrome?
What is the clinical presentation of nephrotic syndrome?

A

In Nephrotic syndrome, there is damage to the podocytes. This leads to scarring, and deposition of matrix and other elements.
Nephrotic syndrome px with a triad of proteinuria (>3g in 24 hrs), or a protein:creatinine ratio of >300-350mg/mmol), hypoalbuminaemia ( albumin <25g/L) and oedema. severe hyperlipideamia is quite common too.
Nephrotic syndrome is associated with minimal change nephropathy, focal segmental glomerulonephritis, membranous nephropathy, amyloid, and diabetic nephropathy.

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24
Q

What is Goodpastures disease?

A

Goodpastures disease is is also known as Anti glomerular basement membrane (GBM) disease. It involves the development of autoantibodies against type IV collagen. It generally results in a nephritic syndrome and generally affects young males. Type four collagen is also found in the lungs and heamoptysis may also be a feature.

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25
Q

What are the life threatening consequences of acute kidney injury?

A

Hyperkaleamia, volume overload, metabolic acidosis

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26
Q

What are the causes of acute kidney injury?

A

PreRenal causes: hypovoleamia, sepsis, CCF, cirrhosis, renal artery stenosis, NSAIDS, or ACE inhibitors ( these interfere with renal artery blood flow).
Intrinsic causes: acute tubular necrosis ( damage to the renal cells caused by ischeamia or nephrotoxins) caused by chemo, drugs, rhabdomyolysis, radiological constrasts or myeloma.
Other: vasculitis, malignant hypertension urinary tract obstruction.

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27
Q

What signs and symptoms Are present for acute renal failure?

A

Oligouria, nausea and vomiting, Orthoptera, hypotension. Pulmonary oedema, dizziness.

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28
Q

Give an example of a loop diuretic. Where does it act and what channel does it act on? How does it affect fluid electrolyte balance? What conditions is it used for?

A

Furosemide (LAsix) is a loop diuretic. It acts on the thick ascending loop of Henle. It blocks the Na/K/2Cl channels. Frusemide causes NaCl excretion and some calcium excretion. It causes dieresis 4 hours after it is given. Furosemide is used to treat oedema in heart failure, ascities, and acute pulmonary oedema.

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29
Q

What are the side effects of loop diuretics?

A

Loop diuretics cause a hypokaleamoc metabolic alkalosis.

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29
Q

What are the side effects of loop diuretics?

A

Loop diuretics cause a hypokaleamoc metabolic alkalosis.

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29
Q

What are the side effects of loop diuretics?

A

Loop diuretics cause a hypokaleamoc metabolic alkalosis.

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32
Q

What percentage of kidney stones are radiopaque? Which are the most visible and which are the least visible?

A

Around 60% though estimates greatly differ. The most is calcium phosphate, then calcium oxalate, then struvite, then Cystic acid and Uric acid

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33
Q

What are the symptoms of kidney stones?

A

Renal colic flank pain radiating to the ipsilateral thigh, nausea and vomiting, rarely heamaturia, possible fever and urinary frequency or urgency. Confirm with an abdominal pelvic X-ray or a helical ct scan

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34
Q

What are the common causes if frank heamaturia ?

A

UTI, kidney stone, pyelonephritis, recent urethral instrumentation, prostate cancer, kidney cancer. Alports syndrome, BPH

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35
Q

What are the hypertensive diseases that cause renal damage?

A

Malignant hypertension. Essential hypertension, preeclampsia

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36
Q

What are the renal causes of hypertension?

A

Diabetic nephropathy, glomerularnephritis, chronic interstitial nephritis, poly cystic kidneys, or renal vascular disease

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37
Q

What is renal vascular disease? What are its causes?

A

Renal vascular disease is renal artery stenosis, or stenosis of one of its branches. The most common causes are atheroma or muscular dysplasia

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38
Q

What drug combination is referred to as the triple whammy?

A

Ace inhibitors or ARBs, NSAIDs, and a diuretic

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39
Q

Why does renal artery stenosis produce hypertension?

A

The hypoperfused kidney responds by increasing levels of renin and angiotensin II

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40
Q

What are the symptoms of renal artery stenosis?

A

Hypertension, possible history of cardiovascular disease or fibromuscular dysplasia, abdominal Brits, flash pulmonary oedema

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41
Q

What is haemolytic ureamic syndrome?

A

Haemolytic ureamic syndrome is a clinical syndrome that comprises of progressive renal failure associated with microangiopathic (Coombes negative, nonimmune) haemolytic aneamia and thrombocytopenia. It is the most common cause of acute renal failure in children. HUS may or may not be associated with shigalike toxin. Whilst it also occurs in adults and can be triggered by many causes, it most commonly occurs in children after an episode of acute diarrhoea.

42
Q

What are the signs and symptoms of HUS?

A 
Prodromal gastroenteritis
Acute renal failure
Anuria
Lethargy or seizures
Hypertension
Oedema
Pallor
43
Q

What tests would you order for HUS? what is the treatment for for HUS?

A

Urinalysis, GFR and creatinine, FBC ( measuring RBCs and platelets), EUC, BP, PT and APTT (normal, peripheral blood smear ( schistocytes), adamst13 (levels are normal in HUS and low in TTP)

44
Q

On what channel and in which area does a thiazides diuretic act? What is its effect? What conditions is it used to treat?

A

Thiazides diuretics act on the distal convuluted tubule on the NaCl channels. It causes the excretion of NaCl, but not of calcium. Hence it is used to prevent the formation of calcium renal stones, as well as a diuretic to reduce blood pressure and sometime to reduce oedema

45
Q

What is thrombotic thrombocytopenia our ours (TTP)?

A

TTP is a rare blood disorder that is characterised by clotting in the small blood vessels of the body resulting in a low platelet count. The full blown condition of this disease consists of microangiopathic haemolytic aneamia, thrombocytopenia purpura, renal disease, neurological abnormalities, and fever.

46
Q

Name two types of potassium sparing diuretics that are aldosterone antagonists. Name two types of postassium sparing diuretics that block sodium channels in the collecting tubules.

A

Two types of potassium sparing diuretics that act as aldosterone antagonists are eplerenone and spironalactone. Two potassium sparing diuretics that act by blocking the sodium channels in the collecting ducts are amiloride and triamterrine.

47
Q

What is the effect of aldosterone?

A

Aldosterone increases sodium conservation, water conservation, and increases blood pressure. It also causes the dumping of potassium

48
Q

What is the effect of potassium soaring diuretics?

A

Potassium spring diuretics increase sodium excretion and decrease K and H excretion. They are used to control the K+wasting caused by long term diuretics

49
Q

What are the risk factors for diabetes insipid us?

A

Pituitary surgery, craniopharyngioma, pituitary stalk lesions, traumatic head injury, autoimmune disorders and use of lithium.

50
Q

What is are the symptoms of diabetes insipid us?

A

Increased thirst, polyuria of dilute hypotonic urine ( normally no hypernateamia as polydipsia adequately replaces fluids)

51
Q

What is diabetes insipid us?

A

Diabetes insipidus is a metabolic disorder characterised by an inability to concentrate urine resulting in hypotonic dulite polyuria. It is either caused by a default in the production of vasopressin ( anti diuretic hormone) which is produced by the hypothalamus and secreted by the kidneys. It may also be due to resistance to ADH on the renal collecting ducts.

52
Q

High pH, low CO2, low bicarbonate

A

Respiratory alkalosis

53
Q

High Ph, high co2, high HCO3

A

Metabolic alkalosis

54
Q

Low pH, low CO2, low hCO3

A

Metabolic acidosis

55
Q

Low pH, high CO2, high bicarbonate

A

Respiratory acidosis

56
Q

Where is renin made? What stimulates renin production?

A

Renin is released from smooth muscle cells in the walls if the afferent and efferent artierioles at the point where they make contact with the early distal tubule ( macula densa). To form the juxtoglomerular apparatus. Renin release is stimulated by reduced perfusion pressure in the afferent arteriole, increased sympathetic nerve activity, decreased sodium chloride conc in the distal tubular fluid.

57
Q

Describe the RAAS

A

Renin is produced by the kidneys in response to signs of hypovoleamia, it acts on angiotensinogen (made in the liver) producing angiotensin 1. Angiotensin1 is cleaved by ACE becoming angiotensin 2 , largely in the pulmonary capillary bed. Angiotensin 2 has multiple actions, including stimulation of the proximal tubular sodium reabsoption, release of aldosterone from the zone glomerulus of the adrenal cortex, and vasoconstriction of small artierioles.

58
Q

How do you assess a hospitalised patient for fluid and electrolyte balance?

A

Examinine the patient for signs of hypovoleamia or hypervoleamia, check daily weight change. Review the fluid balance chart checking total volumes in and out on previous day ( should be approx 400mL positive due to insensible fluid losses), correlate chart figures with weight change and clinical volume status to estimate net fluid balance. Assess ongoing pathology: check losses from GI tract and surgical drains, estimate increased insensible losses eg in fever and internal sequestration. Check plasma and EUC. Plasma Na is a marker of fluid balance, K is a marker of extra cellular K balance. HCO3 is a clue for acid base disorder, urea and creatinine monitor renal function.

59
Q

What are the causes of excessive sodium and water retention?

A

Impaired renal function from primary renal disease, primary hyper aldosteronism ( eg Conns syndrome), secondary hyper aldosteronism from congestive cardiac failure, cirrhosis of the liver, nephrotic syndrome, malnutrition, renal artery stenosis.

60
Q

What is hyponatreamia?

A

Hyponatreamia is a plasma Na <135 mmol/L. It is a common electrolyte abnormality often detected asymptomatically, but also associated with anorexia, nausea, vomiting, confusion, lethargy, seizures, and coma.the patient experiences more symptoms when they have not had time to adjust eg. Acute changes.

61
Q

What are the causes of hypovoleamic hyponatreamia?

A

Renal Na losses, diuretic therapy (especially thiazides), adrenocortical failure, gastrointestinal sodium losses,
Vomiting, diarrhoea, skin Na losses, burns

62
Q

What are the causes of euvoleamic hyponatreamia?

A

Primary polydipsia, excessive electrolyte free water infusion, SIADH, hypothyroidism.

63
Q

What are the causes of SIADH?

A

Tumours ( eg lung or colon cancer)
CNS disorders: stroke, trauma, infection, psychosis.
Pulmonary disorders: pneumonia, tuberculosis, obstructive lung disease
Drugs: anticonvulsants( carbemezapine), psychotropics (haloperidol), antidepressants (amitryptine, fluoxetine), cytotoxics (cyclophosphamide, vincristine) hypoglycaemics, opiates, idiopathic.

64
Q

What is the typical presentation of someone with Crohn’s disease?

A

Typical presentation of Crohn’s disease includes abdo pain (may be cramps, relieved with defection), non bloody or intermittently bloody diarrhoea, perianal lesions (skin tags, fistulae, abscesses, scarring, or sinuses). It may commonly present with bowel obstruction, fever, fatigue, abdo tenderness,

65
Q

What two things should you always check for in acute renal failure?

A

Hypovoleamia and urinary tract obstruction.

66
Q

How do you manage acute renal failure?

A

Enlist specialist help. Whilst waiting, make sure that recent U&E and urine microscopy results that are on hand. Identify and treat the pre renal and post renal causes (obstruction and hypovoleamia). Order an urgent ultrasound scan. You must check for a palpable bladder, but its absence does not rule out obstructive causes. Stop any nephrotic drugs. (NSAIDs, ACEi, gentamicin, vancomycin, amphotericin, stop metformin if creatinine is >150 mmol/L). Check for sis of vasculitis ( nose bleed, heamaturia, rash, ESR/CRP) if there is sis of vasculitis then test for autoantibodies. Monitor pulse, BP, urine output, and CVP hourly (insert a urinary catheter). Correct any volume depletion with IV fluid. Take blood cultures if patient is septic. Remove any possible sources of sepsis when no longer required (eg cannula, catheter). Recheck for any nephrotoxic drugs, adjust doses for any really e created drugs. Aim for normal calorie intake. If oral intake is poor, consider giving TPN.

67
Q

What are the potential complications of acute kidney disease?

A
  • hyperkalemia/ECG changes: IV calcium is cardio protective, IV insulin and glucose to lower potassium (check capillary glucose approx 30mins after). Consider calcium resonium to bind K in the gut. Heamodialysis or heamofiltration required if anuric.
  • Pulmonary oedema: sit up and give high flow oxygen by face mask. Use a venous vasodilator (eg morphine), give fruso die IV over 1 hour, if no response urgent heamodialysis or heamofiltration is needed. Consider CPAP.
  • Bleeding: impaired haemostasis due to increased urea may be compounded by the precipitating cause. Give PPIs or a H2 antagonist. In the case of an active bleed give fresh frozen plasma or platelets as needed. Blood transfusion to maintain Hb >10g/dL and heamotocrit >30%., desmopressin to increase factor VIII activity.
68
Q

What are the indications for acute dialysis?

A

Indications for acute dialysis include refractory pulmonary oedema, persistent hyperkalemia ( K>7mmol/L), severe metabolic acidosis, (pH<7 or base excess <10), ureamic encephalopathy, ureamic pericarditis (pericardial rub).

69
Q

How do you classify renal impairment in chronic kidney disease?

A 
Stage 1   GFR >90
Stage 2   GFR >60
Stage 3a GFR >45
Stage 3b GFR >30
Stage 4   GFR >15
Stage 5   GFR <15
Stage 1 and 2 must be accompanied by other symptoms suggesting renal damage such as proteinuria, heamaturia, or other evidence of renal disease.
70
Q

What is end stage renal failure?

A

End stage renal failure is defined as stage 5 renal failure (GFR<15), or need for renal replacement therapy (dialysis or transplant).

71
Q

What are the symptoms of chronic renal failure?

A

Fatigue, weakness, metallic taste in mouth, anorexia, vomiting, pruritis, restless legs, bone pain, impotence/infertility. Symptoms are common when urea is >40mmol/L. Such as dyspnoea or fluid overload.

72
Q

Who should be screened for chronic renal failure?

A

High risk groups should be screened for chronic renal failure: DM, HTN, age>60, recurrent UTIs, urinary obstruction, or a systemic illness that affects the kidneys (eg SLE), cardiovascular disease (IHD, CCF, peripheral vascular disease, or cerebral vascular disease and cerebral vascular disease), structural renal tract disease, renal stones, BPH, family history of stage 5 CRF or inherited renal disease.

73
Q

What are signs found upon examination of a patient with chronic renal failure?

A

Yellow skin, brown nails, excoriation, hypertension, pallor, bruising. Increased BP, cardiomegaly, pericardial rub, pleural effusion. Pulmonary or peripheral oedema, proximal myopathy. If untreated may also present with arrhythmias, encephalopathy, seizures, and coma.

74
Q

What is acute tubulointerstitual nephritis?

A

Tubulointerstitual nephritis is inflammation of the renal interstitium. It may be acute or chronic. Acute tubulointerstitual nephritis is mediated by an immune reaction to medications, infections and other causes. It may present with renal impairment, HTN, or ARF. May also have systemic symptoms such as fever, rash, arthralgia, with eosinophilia, uveitis, and increased IgE.

75
Q

What is minimal change nephropathy?

A

Minimal change nephropathy is the most common cause of nephrotic syndrome in young adults/children. Most cases are idiopathic, but in 10% there is a cause (Drugs, Hodgekin’s lymphoma, thymoma, mononucleosis).T cells and cytokines attack the glomerular basement membrane, reducing the electrostatic charge, increasing permeability to albumin Presentions with neprotic syndrome and normal blood pressure. Manage with steroids. Prognosis is good..

76
Q

What is chronic tubulointerstitual nephritis?

A

Chronic tubulointerstitual nephritis is chronic inflammation of the renal interstitium. It results from many disorders, leading to extensive fibrosis and tubular loss on renal biopsy. Patients present with chronic renal failure. Causes include chronic pyelonephritis often with reflux nephropathy, sickle cell disease, lead or cadmium intoxication.

77
Q

What is Balkan Nephropathy?

A

Balkkan Nephropathy is a chronic tubulointerstitual disease associated with a high frequency of urothelial atypia occasionally culminating in tumours of the renal pelvis and urethra. It occurs in people living along the Danube River.

78
Q

What is analgesic nephropathy?

A

Analgesic nephropathy is associated with the prolonged heavy ingestion of analgesics (particularly NSAIDs, paracetamol, and penacetin). The ingestion of analgesics leads to interstitial nephritis and papillary necrosis. There is often a history of chronic pain. In analgesic nephropathy there is a slow progression to chronic renal failure. Proteinuria or sterile pyuria.

79
Q

What is sterile pyuria?

A

Sterile pyuria is the finding of elevated white cells in a urine sample in which no infection is found. It is found in UTIs and renal disease.

80
Q

What is urate nephropathy?

A

Urate Nephropathy can be either acute crystal nephropathy or chronic crystal nephropathy. In acute crystal nephropathy there is acute oliguric or anuric renal failure due to uric acid precipitation in the tubules. It is most often due to the overproduction of uric acid in patients with lymphoma, leukaemia, or a myeloproliferative disease. The renal parenchyma appears bright on Ultrasound. There are also cases of chronic urate nephropathy.

81
Q

Which diseases cause hypercalceamia?

A

Hypercalceamia is caused by nephrogenic diabetes insipidus, renal calculi, and nephrocalcinosis (diffuse renal parenchymal calcification, often asymptomatic, causing progressive renal impairment).

82
Q

What is Rhabdomyolysis?

A

Rhabdomyolysis results from skeletal muscle breakdown, with release of its contents into circulation (myoglobin, K, PO4, urate, and creatinine kinase). Comlications include hyperkalaemia and acute renal failure. ARf is cuased by the myoglobulin being filtered through the glomeruli and obstructing the renal tubules. Causes can be divided into: Post Ischeamic (embolism, clamp on artery during surgery), Trauma(prolonged immobilisation, burns, crash injury, excessive exercise, uncontrolled seizures), Drugs and Toxins (statins, fibrates, EtOH, ectasy, heroin, neuroleptic malignant syndrome), Infections, and inherited muscle disorders.

83
Q

What are the clinical features of Rhabdomyolysis?

A

Clinical features of rhabdomyolysis include muscle swelling, pain, tenderness, and red-brown urine (myoglobinuria). Plasma shows increased creatine kinase, and MI must be excluded as a cause. Associated with compartment syndrome, hyperkalaemia, and DIC.

84
Q

Which renal diseases are most commonly associated with causing hypertension?

A

Diabetic nephropathy, glomerulonephritis, chronic interstitial nephritis, polycystic kidney disease or renovascular disease.

85
Q

How do you treat hyperkalaemia?

A

Treat the underlying cause (eg. acute renal failure) and stop any exacerbating drugs (eg. ACE Inhibitors).

  • Stabilise the cardiac membrane (IV Calcium Gluconate)
  • Short term shift from extracellular to intracellular Potassium (combined insulin/dextrose infusion, nebulised salbutamol)
  • Remove Potassium from the body (Calcium Resonium, loop diuretics, dialysis).
86
Q

What is renal vascular disease?

A

Renal Vascular disease is stenosis of the renal artery or one of its branches. It is most commonly caused by atherosclerosis in older patients, or fibromuscular dysplasia in younger patients. Clinically, there is hypertension that is resistant to treatment, worsening renal function after ACE inhibitors in bilateral renal artery stenosis, ‘flash’ pulmonary oedema, sudden onset LV hypertrophy on echo. Abdo and carotid femoral bruits, and weak leg pulses may be found. Ix: Ultrasound, CT MR, renal angiography.

87
Q

What is renal tubular acidosis?

A

Renal tubular acidosis is metabolic acidosis due to impaired acid secretion by the kidney.

88
Q

What is type one RTA?

A

Type 1 Renal Tubular Acidosis is distal. It is due to an inability to excrete hydrogen ions and generate acidic urine in the distal tubule, even in states of metabolic acidosis. Causes include idiopathic, genetic (Marfan’s, Ehlers-Danlos), Autoimmune (SLE, Sjorgrens, Autoimmune hepatitis), Nephrocalcinosis, Tubulointerstitual disease, or drugs.

89
Q

What is type two Renal Tubular Acidosis?

A

Type Two renal tubular acodisis occurs proximally and is due to ‘bicarbonate leak’. It is a defect in the bicarbonate reabsorption in the proximal tubule resulting in excess bicarbonate in the urine. Causes of type two renal tubular acidosis include Idiopathic, Fanconi’s syndrome, Tubulointerstitual disease (myeloma, interstitial nephritis), and drugs.

90
Q

What is Fanconi Syndrome?

A

The proximal tubule is responsible for reabsorption of many solutes, including 50% of filtered sodium, most bicarbonate, and all filtered glucose and amino acids. Fanconi’s Syndrome is a disturbance of the proximal tubule function, with defective resorption of amino acids, potassium, phosphate (leading to hypophosphateamic rickets and osteomalacia), glucose (glucosuria), and bicarbonate (type 2 RTA) There is also polyuria and hypokalaemia. Can be idiopathic, inherited, or acquired from tubule damage.

91
Q

What is Polycystic Kidney Disease?

A

Polycystic kidney disease is an inherited disorder involved PKD1, and PKD2. It presents with renal enlargement with cysts, abdominal pain +/- haematuria, cyst infection, renal calculi, hypertension, and progressive renal failure. May also present with liver cysts and intracranial aneurysms.

92
Q

How do you manage chronic renal failure?

A

Control Hypertension. Target BP is <45mL/min.
Manage CVD risk by giving statins and aspirin.
Manage severe anaemia by excluding other causes and giving EPO.
Treat osteodystrophy if high PTH.
Oedema can be treated with frusemide and fluid and sodium restriction.
Restless legs can be treated with clonazepam or gabapentin. Bicarbonate supplements may be needed to correct acidosis.

93
Q

What is haemodialysis?

A

In haemodialysis, blood flows on one side of a semi-permeable membrane while dialysis fluid flows in the opposite direction on the other side. solute transfer occurs by diffusion. Small solutes (eg. urea) diffuse readily, while larger solutes diffuse less readily and are not cleared as effectively. Ultrafiltration is the removal of excess fluid by creating negative transmembrane pressures.

94
Q

What problems are associated with heamodialysis?

A

Problems associated with haemodialysis include disequilibriation syndrome (caused by rapid changes in plasma osmolarity and cerebral oedema caused by dialysis). Hypotension, arrhythmias, Time consuming. Access issues surrounding the fistula include thrombosis, stenosis, aneurysm, steal syndrome and ischeamia. Temporary sites may have problems with infection or blockage.

95
Q

What is heamofiltration?

A

In heamofiltration, blood is filtered across a highly permeable membrane allowing removal of waste products via a process of convection. Compared with diffusion, convection moves larger solutes almost at the same rate as smaller solutes. The ultrafiltrate is replaced with an equal volume of replacement fluid. It is more expensive and takes longer than HD, but there is less heamodynamic instability and so it is used for critically ill patients.

96
Q

What is peritoneal dialysis?

A

Peritoneal dialysis is simple to perform, requires less complex equipment, and can be completed at home. It is useful in children, the elderly, and those with cardiovascular disease. PD fluid is introduced into the peritoneal cavity via the Tenchkoff catheter and ureamic solutes diffuse into it across the peritoneal membrane. Ultrafiltration is achieved by adding osmotic agents eg. glucose to dialysis fluid.

97
Q

What are the problems associated with peritoneal dialysis?

A

Peritoneal dialysis is associated with peritonitis (60%staphlococci). there is also exit site infection, catheter malfunction, Loss of membrane function, Obesity (glucose in dialysis fluid), hernias, and back pain.

98
Q

What are the common complications that occur in dialysis patients?

A 
Cardiovascular disease (IHD, cardiac failure, and stroke), anaemia, Protein-Calorie Malnutrition, Platelet dysfunction causing a tendency to bleed, renal osteodystrophy, infection (uraemia causes granulocyte dysfunction). 
Beta2 macroglobulin amyloidosis is due to amyloid accumulation in long term dialysis patients, causes carpal tunnel, arthralgia, and fractures.
Acquired Renal Cysts occur after years of dialysis and may present with haematuria or malignant transformation. Malignancy has also been found to be more common in dialysis patients, but this may be due to the cause.
99
Q

What are the contraindications to renal transplant?

A

Active infection, severe heart disease, cancer and other severe comorbidity. Previous TB may reactivate so it must be treated. HEP B and C, CMV, HIV, EBV, and varicella zoster may cause severe disease whilst immunocomprimised.

100
Q

What are the different graft type options for renal transplantation?

A

Cadaveric donor, non heart beating donors, living related donor, live unrelated donation.

101
Q

What immunosuppression therapy is used in renal transplantation?

A 
Most regimes involve:
1. Ciclosporin or tacrolimus, and
2. azathioprine or mycophenalate, +/-
3. Prednisolone.
Pre-op receives anti-interleukin 2 receptor antibodies (eg. basiliximab) to reduce rates of early rejection.
102
Q

What are the complications of renal transplant?

A

Acute: bleeding, thrombosis, infection, urinary leaks, oligouria, acute rejection.
Chronic: Chronic rejection, Infection related to immunosuppression, ciclosporin/tacrolimus toxicity, increased chance of malignancy, atheromatous vascular disease, and hypertension.

Medicine (16 decks)

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