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Stage 4 CSIM > Abnormal Renal Fuunction > Flashcards

Abnormal Renal Fuunction Flashcards

1
Q

Approximately, what is a normal GFR?

A

120-130mL/min

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2
Q

Describe the different roles the kidney has in the body, and what may be affected if kidney function goes off?

A 
EXCRETORY
waste products and drugs
REGULATORY
fluid volume and composition
ENDOCRINE
epo, renin, protaglandins
METABOLIC
vitamin D and some proteins
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3
Q

Describe some of the features of NEPHROTIC syndrome

A

PROTEINURIA
+++ protein on dipstick
urine looks ‘frothy’
HYPOALBUMINAEMIA
Decreased vascular oncotic pressure - oedema
HYPERLIPIDAEMIA
Side effect of increased albumin production in liver

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4
Q

Describe some features of NEPHRITIC syndrome

A 
HAEMATURIA 
\+++ blood on dipstick
may be micro or macroscopic 'coca-cola coloured'
red cells clasts on microscopy = distinguishing feature
PROTEINURIA
\+/++ small amount
HYPERTENSION 
usually only mild
POOR URINE OUTPUT 
usually
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5
Q

At what site are transplanted kidneys put in the abdomen?

A

Iliac Fossa

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6
Q

If protein was present on urine dipstick, how would we quantify the leak?

A

Urine Albumin Creatinine Ratio (UACR)

Urine Protein Creatinine Ration (UPCR)

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7
Q

What imaging modalities are available to look at the kidneys?

A

FIRST LINE = ultrasound (+/- Doppler for blood flow)
AXR KUB for calcification/stones
IVP - although now largely replaced by CT
MRI
Nuclear Medicine e.g. DMSA for scarring

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8
Q

How is nephrotic syndrome defined?

A

> 3.5g/24 hour urine

UPCR >300

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9
Q

What is the most common pathogen causing UTI in community and hospital?

A

E.Coli

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10
Q

In a patient who presents with recurrent disabling UTIs can anything be done to help prevent them?

A

Low dose, once daily prophylactic antibiotics
For a limited period of time, usually 1-2 years, after which treatment should be stopped and the patient reassessed.
Also single dose post-coital antibiotics can be effective, particularly if infections follow intercourse

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11
Q

List the ways in which microscopic vasculitis may present.

A

CONSTITUTIONAL
fever, night sweats, anorexia, malasie, weight loss
ORGANS
Episcleritis, skin rashes, joint pains, nose bleeds, GI bleeding, AKI, CKD, pulmonary haemorrhage, mononeuritis multiplex (nerve damage), seizures due to intracerebral haemorrhage.

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12
Q

Why do you give co-trimoxazole to anyone who is receiving immunosupression with cyclophosphamide?

A

As PCP prophylaxis

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13
Q

In simple terms what are the 2 causes of haematuria?

A

Bleeding from anywhere along the urinary tract

Leaky glomerulus

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14
Q

List the non-proliferative glomerulonephritises that cause NEPHROTIC syndrome

A

Minimal Change GN
Membranous GN
Focal Segmental GN

N.B. lack of proliferation in cells of glomeruli

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15
Q

Describe the salient points of Minimal Change GN

A

Presents as nephrotic syndrome (proteinuria –> frothy, hypoalbuminaemia –> oedema, hyperlipidaemia)
Nomral light, but fused podocytes on electron microscopy
Cause unknown (80% GN in children, 20% adults)
Give prednisolone to halt disease progression - 90% respond well, cured at 3 months

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16
Q

Describe the salient points of Focal Segmental GN

A

Presents as nephrotic syndrome (proteinuria –> frothy, hypoalbuminaemia –> oedema, hyperlipidaemia)
Caused by specific segments of glomeruli developing sclerotic lesions, can be primary (genetic mutations) or secondary (to HIV, reflux nephropathy).
ALL ANTIBODIES NEGATIVE
50% progress to renal failure - transplant, steroids ineffective, supportive Rx.

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17
Q

Describe the salient points of Membranous GN

A

Presents as nephrotic syndrome (proteinuria –> frothy, hypoalbuminaemia –> oedema, hyperlipidaemia)
Immune complex deposition, complement activation against basement membrane - thickened basement membrane and IgG deposition seen.
Usually idiopathic, usually affects 30-50 yr olds
Prognosis - rule of thirds
1/3 chronic membranous GN, 1/3 remission, 1/3 end stage renal failure. Can give steroids if progresses.

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18
Q

List the Glomerulonephritises that can result in NEPHRITIC SYNDROME.

A

IgA Nephropathy
Post-Infectious Nephropathy
Membranoproliferative
RAPIDLY PROGRESSIVE GN (cresenteric) which includes
Good Pastures
Vasculitis - Wegeners, Microscopic Polyangitis

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19
Q

Describe the salient points of IgA Nephropathy

A

Most common GN in adults worldwide
Presents as NEPHRITIC SYNDROME - macroscopic Haematuria
Often appears 24-48 hours after URTI
Microscopy - increase numbers of mesangial cells, Increased matrix with IgA deposited in matrix
Episodes occur randomly for a few months - stops in 80%, 20% go on to develop end stage renal failure

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20
Q

Describe the salient points of Post-Infectious Glomerulonephritis

A

Usually 2 weeks after strep pyogenes (GAS) infection (although can be any infection)
Diagnosis - symptoms and signs of nephritic syndrome, Hx of strep infection, strep titres may help
Microscopy - increase mesangial cells, neutrophils and monocytes, bowman space is compressed.
Usually resolves in 2-4 weeks

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21
Q

Describe the salient points of Membranoproliferative Glomerulonephritis

A

Combined nephrotic and nephritic syndrome
Mesangium AND basement membrane thickened.
Can be primary or secondary to SLE, hepatiitis
Linear pattern of IgG deposition, in lupus nephritis get “full house immune deposition”
Most progress to end stage renal failure - poor prognosis

22
Q

Describe rapidly progressive glomerulonephritis and its causes

A

Also known as cresenteric glomeurlonephritis.
Poor prognosis - rapid progression to kidney failure over weeks
Any form of glomerulonephritis can progress to RPGN but some forms only ever present this way
Including Gooodpastures Syndrome and the Vasculitises e.g. wegeners and microscopic polyangitis

23
Q

Describe the salient points of Goodpastures Syndrome

A

Anti GMB antibodies - located in glomeruli and alveoli
Patients present with nephritic syndrome and renal failure and also haemoptysis
Get linear IgG deposits along glomerular basement membrane
High dose immunosupression required, kidney damage already done is irreversible

24
Q

Describe the salient points of Wegeners Granulomatosis

Granulomatosis with c-ANCA positive polyangitis

A

c-ANCA positive
Affects lungs, kidneys and other organs
Tx - Iv steroids and cyclophosphamide

25
Q

Describe the salient points of Microscopic Polyangitis

A

Small vessel vasculitis - can affect almost any organ system
p-ANCA positive
Tx - steroids and cyclophosphamide

26
Q

What investigations would you do to diagnose glomerular disease?

A

Urine Dipstick (blood +++, protein +++)
Microscopy to pick up red cell clasts
Auto-antibody screen - anti GMB, p-ANCA, c-ANCA
Biopsy with microscopy and immunohistochemistry and immunoflourescence.

27
Q

Describe the consequences of sudden loss of renal function

A

ACCUMULATION OF TOXINS
urea - N & V, malaise, pericarditis, pleurisy, fitting, increase bleeding and infection risk
Metabolic Acidosis - haemodynamic instability, disruption of cellular function
Potassium - muscle weakness, cardiac instability
ACCUMULATION OF SALT AND WATER
Fluid Overload - hypertension, oedema - pulmonary, pedal, facial

28
Q

How is an AKI defined?

A

ANY ONE OF THE FOLLOWING
Increase of serum creatinine by >26.5mmol/L in 24 hours
Increase in serum creatinine by >1.5x baseline
Urine Volume

29
Q

List ways you can tell an AKI from other causes of poor renal function

A

Previous Bloods to compare change in creatinine to
Ultrasound kidneys (CKD kidneys will be smaller)
Duration of Symptoms
Discrete Insult

30
Q

The cause of AKI can be split into 3 catergories, what are they?

A

Pre-Renal Azotaemia
Intrinsic AKI
Post-Renal AKI

31
Q

The cause of post renal AKI is essentially urinary obstruction, what can cause this and how should it be screened for?

A

Young Patients - Renal Stones
Older Patients - renal stones, prostatic hypertrophy or carcinoma, retro peritoneal or pelvic neoplasms.
Screen by asking patients about urinary symptoms, when they last passed urine
palpate the abdomen for a full bladder
Renal Ultrasound - hydronephrosis

32
Q

Why is it called pre-renal azotaemia?

A

Azotaemia = build up of nitrogenous waste compounds in the blood
In pre-renal no renal cell injury has yet occured, so why some nephrologists say azotamiea opposed to AKI

33
Q

Describe the pathophysiology of pre-renal AKI?

A

It is an APPROPRIATE RESPONSE to kidney hypoperfusion
Usually kidney is able to maintain GFR close to normal despite wide variations in renal perfusion = AUTOREGULATION
However, too large a drop in perfusion leads to decreased GFR and development of pre-renal uraemia
This may eventually lead to established parencyhmal liver injury and development of AKI.

34
Q

Describe the treatment of pre-renal AKI and why patients should be monitored very closely.

A

Tx - prompt fluid replacement to restore renal perfusion
However, since renal parenchymal damage may already have begun to occur, should monitor patients very closely as fluid challenge may lead to volume overload with pulmonary oedema
Check BP regularly, and look for signs of JVP and auscultate chest for pulmonary oedema.

35
Q

Describe the mechanism by which NSAIDs and ACE inhibitors can contribute to development of AKI

A

NSAIDs
Stop production of vasodilatory prostoglandins that act on afferent arteriole
ACE inhibitors
Stop production of vasconstricting angiotensin II =, which acts on efferent arteriole
Loss of this pressure gradient, means glomerular filtration isn’t ‘pushed’ as much, slows down GFR
Rarely the sole cause of AKI but can compound existing pathology

36
Q

Describe the salient points of acute tubular necrosis

A

One of the most common causes of AKI
Results most commonly from renal ischaemia, also be caused by direct renal toxins e.g drugs, myoglobin, radiocontrast
Urinalysis usually normal but can see
Epithelial cell clasts on microscopy - pathognomonic
Clinical course is variable depending on severity and duration of insult
Recover of renal function is usually at 7-21 days - as tubular cells continually replace themselves

37
Q

Describe the salient points of acute allergic interstitial nephritis

A

Most commonly caused by allergic reaction to a drug - can see fever, rash and enlarged kidneys
Can also be caused by other kidney diseases e.g. Pyelonephritis
Again urinalysis usually normal

38
Q

How can the urinary sodium help to distinguish between pre-renal AKI vs ATN

A

Pre-renal AKI - urinary sodium 40

39
Q

List some of the common indications for renal biopsy

A

Protein +++ and Blood +++ on Dipstick
Any suspicion of RPGN
If pre-renal AKI, post renal AKI or ATN cannot be confidently diagnosed to find the cause of AKI

40
Q

How does weight loss correspond to improvement in blood pressure?

A

5-10mmHg per 10kg weight loss

41
Q

What lifestyle advice should be offered to someone who presents with hypertension?

A 
Maintain normal weight/weight loss
Reduce salt intake
Regular exercise 
Limit alcohol consumption
Stop smoking 
Reduce intake of fat and increase intake of fruit and veg
42
Q

How can renal disease cause secondary hypertension?

A

Hypoperfusion leads to hyperactivation of the renin-angiotensin-aldosterone axis, causing hypertension
Intrinsic Renal Disease - 75% of cases
Renovascular Disease - 25% of cases

43
Q

What are the common causes of renovascular disease?

A

Atherosclerosis - >90% of cases in white vascular high risk populations
In India - Takayasu’s arteritis is reponsible for aboout 60% of cases
Fibromuscular dysplasia - commonly affects young women 30-40 years
Majority of cases unilateral

44
Q

How might hypertension due to renovascular disease present?

A

Abrupt onset of hypertension
severe hypertension
refractory hypertension
hypertension developing in a person with known vascular disease
hypertension in a person with no family hx of hypertension
renal impairement during treatment with ACE inhibitors or ARBs
De novo renal impairement in a patient with hypertension/normotension with vascular risk factors
hypertension with unexplained hypokalaemia

45
Q

When should a patient be referred to secondary care for investigation of renal artery stenosis?

A

Refractory Hypertension
Recurrent episodes of pulmonary oedema
Rising serum creatinine concentration
Unexplained hypokalaemia with hypertension

46
Q

What is a Duplex Renal Ultrasound Scan?

A

Ultrasound + Doppler

47
Q

What imaging investigations can be done to assess renovascular disease

A

Ultrasound - diagnosis suggested if significant difference in renal size, not diagnostic
Duplex Renal Ultrasound - can be a good diagnostic test
Conventional Angiography - if very high suspsicon, therapy can be carried out at the same time
CT angiography - risk of contrast associated nephropathy
MR angiography - only validated for disease in proximal artery

48
Q

List some of the common causes of chronic kidney disease

A 
Diabetes
Hypertension and Atherosclerosis
Glomerular Disease
Urinary Obstruction
Inherited Disease ADPKD
49
Q

What are the 5 stages of CKD?

A 
STAGE 1 GFR 90+
STAGE 2 GFR 60-90
STAGE 3 GFR 30-60
STAGE 4 GFR 15-30
STAGE 5 GFR
50
Q

What is the pathophysiology of CKD progression?

A

Primary Renal Disease and proteinuria
Leads to loss of nephrons
You get increased blood flow to surviving glomeruli
Leading to increased filtration and pressure in surviving glomeruli
And damage to surviving glomeruli

51
Q

List ways in which the progression of CKD can be slowed

A

Treat underlying cause if possible

BP control

52
Q

What are the symptoms of CKD?

A

Asymptomatic unless significant loss in renal function i.e. Stage 4/Stage 5 disease (GFR

Stage 4 CSIM (9 decks)

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