Abnormal Renal Fuunction Flashcards
Approximately, what is a normal GFR?
120-130mL/min
Describe the different roles the kidney has in the body, and what may be affected if kidney function goes off?
EXCRETORY waste products and drugs REGULATORY fluid volume and composition ENDOCRINE epo, renin, protaglandins METABOLIC vitamin D and some proteins
Describe some of the features of NEPHROTIC syndrome
PROTEINURIA
+++ protein on dipstick
urine looks ‘frothy’
HYPOALBUMINAEMIA
Decreased vascular oncotic pressure - oedema
HYPERLIPIDAEMIA
Side effect of increased albumin production in liver
Describe some features of NEPHRITIC syndrome
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
At what site are transplanted kidneys put in the abdomen?
Iliac Fossa
If protein was present on urine dipstick, how would we quantify the leak?
Urine Albumin Creatinine Ratio (UACR)
Urine Protein Creatinine Ration (UPCR)
What imaging modalities are available to look at the kidneys?
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
How is nephrotic syndrome defined?
> 3.5g/24 hour urine
UPCR >300
What is the most common pathogen causing UTI in community and hospital?
E.Coli
In a patient who presents with recurrent disabling UTIs can anything be done to help prevent them?
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
List the ways in which microscopic vasculitis may present.
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.
Why do you give co-trimoxazole to anyone who is receiving immunosupression with cyclophosphamide?
As PCP prophylaxis
In simple terms what are the 2 causes of haematuria?
Bleeding from anywhere along the urinary tract
Leaky glomerulus
List the non-proliferative glomerulonephritises that cause NEPHROTIC syndrome
Minimal Change GN
Membranous GN
Focal Segmental GN
N.B. lack of proliferation in cells of glomeruli
Describe the salient points of Minimal Change GN
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
Describe the salient points of Focal Segmental GN
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.
Describe the salient points of Membranous GN
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.
List the Glomerulonephritises that can result in NEPHRITIC SYNDROME.
IgA Nephropathy
Post-Infectious Nephropathy
Membranoproliferative
RAPIDLY PROGRESSIVE GN (cresenteric) which includes
Good Pastures
Vasculitis - Wegeners, Microscopic Polyangitis
Describe the salient points of IgA Nephropathy
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
Describe the salient points of Post-Infectious Glomerulonephritis
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
Describe the salient points of Membranoproliferative Glomerulonephritis
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
Describe rapidly progressive glomerulonephritis and its causes
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
Describe the salient points of Goodpastures Syndrome
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
Describe the salient points of Wegeners Granulomatosis
Granulomatosis with c-ANCA positive polyangitis
c-ANCA positive
Affects lungs, kidneys and other organs
Tx - Iv steroids and cyclophosphamide
Describe the salient points of Microscopic Polyangitis
Small vessel vasculitis - can affect almost any organ system
p-ANCA positive
Tx - steroids and cyclophosphamide
What investigations would you do to diagnose glomerular disease?
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.
Describe the consequences of sudden loss of renal function
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
How is an AKI defined?
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
List ways you can tell an AKI from other causes of poor renal function
Previous Bloods to compare change in creatinine to
Ultrasound kidneys (CKD kidneys will be smaller)
Duration of Symptoms
Discrete Insult
The cause of AKI can be split into 3 catergories, what are they?
Pre-Renal Azotaemia
Intrinsic AKI
Post-Renal AKI
The cause of post renal AKI is essentially urinary obstruction, what can cause this and how should it be screened for?
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
Why is it called pre-renal azotaemia?
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
Describe the pathophysiology of pre-renal AKI?
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.
Describe the treatment of pre-renal AKI and why patients should be monitored very closely.
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.
Describe the mechanism by which NSAIDs and ACE inhibitors can contribute to development of AKI
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
Describe the salient points of acute tubular necrosis
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
Describe the salient points of acute allergic interstitial nephritis
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
How can the urinary sodium help to distinguish between pre-renal AKI vs ATN
Pre-renal AKI - urinary sodium 40
List some of the common indications for renal biopsy
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
How does weight loss correspond to improvement in blood pressure?
5-10mmHg per 10kg weight loss
What lifestyle advice should be offered to someone who presents with hypertension?
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
How can renal disease cause secondary hypertension?
Hypoperfusion leads to hyperactivation of the renin-angiotensin-aldosterone axis, causing hypertension
Intrinsic Renal Disease - 75% of cases
Renovascular Disease - 25% of cases
What are the common causes of renovascular disease?
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
How might hypertension due to renovascular disease present?
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
When should a patient be referred to secondary care for investigation of renal artery stenosis?
Refractory Hypertension
Recurrent episodes of pulmonary oedema
Rising serum creatinine concentration
Unexplained hypokalaemia with hypertension
What is a Duplex Renal Ultrasound Scan?
Ultrasound + Doppler
What imaging investigations can be done to assess renovascular disease
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
List some of the common causes of chronic kidney disease
Diabetes Hypertension and Atherosclerosis Glomerular Disease Urinary Obstruction Inherited Disease ADPKD
What are the 5 stages of CKD?
STAGE 1 GFR 90+ STAGE 2 GFR 60-90 STAGE 3 GFR 30-60 STAGE 4 GFR 15-30 STAGE 5 GFR
What is the pathophysiology of CKD progression?
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
List ways in which the progression of CKD can be slowed
Treat underlying cause if possible
BP control
What are the symptoms of CKD?
Asymptomatic unless significant loss in renal function i.e. Stage 4/Stage 5 disease (GFR
