Abnormal Renal Fuunction

Question 1

Approximately, what is a normal GFR?

Answer 1

120-130mL/min

Question 2

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

Answer 2

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

Question 3

Describe some of the features of NEPHROTIC syndrome

Answer 3

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

Question 4

Describe some features of NEPHRITIC syndrome

Answer 4

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

Question 5

At what site are transplanted kidneys put in the abdomen?

Answer 5

Iliac Fossa

Question 6

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

Answer 6

Urine Albumin Creatinine Ratio (UACR)

Urine Protein Creatinine Ration (UPCR)

Question 7

What imaging modalities are available to look at the kidneys?

Answer 7

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

Question 8

How is nephrotic syndrome defined?

Answer 8

> 3.5g/24 hour urine

UPCR >300

Question 9

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

Answer 9

E.Coli

Question 10

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

Answer 10

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

Question 11

List the ways in which microscopic vasculitis may present.

Answer 11

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.

Question 12

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

Answer 12

As PCP prophylaxis

Question 13

In simple terms what are the 2 causes of haematuria?

Answer 13

Bleeding from anywhere along the urinary tract

Leaky glomerulus

Question 14

List the non-proliferative glomerulonephritises that cause NEPHROTIC syndrome

Answer 14

Minimal Change GN
Membranous GN
Focal Segmental GN

N.B. lack of proliferation in cells of glomeruli

Question 15

Describe the salient points of Minimal Change GN

Answer 15

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

Question 16

Describe the salient points of Focal Segmental GN

Answer 16

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.

Question 17

Describe the salient points of Membranous GN

Answer 17

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.

Question 18

List the Glomerulonephritises that can result in NEPHRITIC SYNDROME.

Answer 18

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

Question 19

Describe the salient points of IgA Nephropathy

Answer 19

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

Question 20

Describe the salient points of Post-Infectious Glomerulonephritis

Answer 20

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

Question 21

Describe the salient points of Membranoproliferative Glomerulonephritis

Answer 21

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

Question 22

Describe rapidly progressive glomerulonephritis and its causes

Answer 22

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

Question 23

Describe the salient points of Goodpastures Syndrome

Answer 23

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

Question 24

Describe the salient points of Wegeners Granulomatosis

Granulomatosis with c-ANCA positive polyangitis

Answer 24

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

Question 25

Describe the salient points of Microscopic Polyangitis

Answer 25

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

Question 26

What investigations would you do to diagnose glomerular disease?

Answer 26

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.

Question 27

Describe the consequences of sudden loss of renal function

Answer 27

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

Question 28

How is an AKI defined?

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

Pre-Renal Azotaemia Intrinsic AKI Post-Renal AKI

Question 31

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

Answer 31

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

Question 32

Why is it called pre-renal azotaemia?

Answer 32

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

Question 33

Describe the pathophysiology of pre-renal AKI?

Answer 33

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.

Question 34

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

Answer 34

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.

Question 35

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

Answer 35

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

Question 36

Describe the salient points of acute tubular necrosis

Answer 36

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

Question 37

Describe the salient points of acute allergic interstitial nephritis

Answer 37

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

Question 38

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

Answer 38

Pre-renal AKI - urinary sodium 40

Question 39

List some of the common indications for renal biopsy

Answer 39

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

Question 40

How does weight loss correspond to improvement in blood pressure?

Answer 40

5-10mmHg per 10kg weight loss

Question 41

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

Answer 41

``` 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 ```

Question 42

How can renal disease cause secondary hypertension?

Answer 42

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

Question 43

What are the common causes of renovascular disease?

Answer 43

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

Question 44

How might hypertension due to renovascular disease present?

Answer 44

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

Question 45

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

Answer 45

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

Question 46

What is a Duplex Renal Ultrasound Scan?

Answer 46

Ultrasound + Doppler

Question 47

What imaging investigations can be done to assess renovascular disease

Answer 47

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

Question 48

List some of the common causes of chronic kidney disease

Answer 48

``` Diabetes Hypertension and Atherosclerosis Glomerular Disease Urinary Obstruction Inherited Disease ADPKD ```

Question 49

What are the 5 stages of CKD?

Answer 49

``` STAGE 1 GFR 90+ STAGE 2 GFR 60-90 STAGE 3 GFR 30-60 STAGE 4 GFR 15-30 STAGE 5 GFR ```

Question 50

What is the pathophysiology of CKD progression?

Answer 50

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

Question 51

List ways in which the progression of CKD can be slowed

Answer 51

Treat underlying cause if possible | BP control

Question 52

What are the symptoms of CKD?

Answer 52

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