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Renal Flashcards

1
Q

What is AKI?

A

Abrupt decline in actual GFR (days to weeks), upset of ECF volume, electrolyte and acid/base homeostasis, accumulation of nitrogenous waste products.

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2
Q

What are the risk factors for AKI?

A
  • CKD
  • Other organ failure especially heart failure, liver disease and diabetes
  • History of AKI
  • Use of nephrotoxic drugs
  • Use of iodinated contrast agents in the last week
  • Over 65 years
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3
Q

What are the prerenal causes of AKI?

A

Pre-renal failure (dehydration most common) – blood supply compromised
• Volume depletion (diarrhoea vomiting etc.)
• Heart failure
• Liver Cirrhosis
• Renal artery atherosclerosis

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4
Q

What are the intrinsic renal causes of AKI?

A

Intrinsic renal failure – damage to glomeruli, renal tubules or interstitium
• Glomerulonephritis
• Acute tubular necrosis – most common cause in clinical practice – Causes: Ischaemia such as shock or sepsis and Nephrotoxins such as aminoglycosides, myoglobin (rhabdomyolysis), radiocontrast agents and lead
• Acute interstitial nephritis
• Intrarenal obstruction such as rhabdomyolysis
• Tumour lysis syndrome

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5
Q

What are the post renal causes of AKI?

A

Post renal failure – obstruction to drainage of both kidneys or a single working kidney
• Stones, blood clots and tumours
• Benign prostatic hyperplasia
• External compression of ureter

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6
Q

How is sodium dealt with by the kidneys during AKI and as it progresses?

A

During early stages of AKI pre-renal uraemia will be seen where the kidneys try to hold onto sodium to preserve circulating volume and so renal perfusion. As kidney function deteriorates into acute tubular necrosis the kidney loses this ability causing a frank loss of sodium.

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7
Q

What are the clinical features of AKI?

A

Usually, asymptomatic
Decreased urine output and extremely concentrated urine
Fluid retention and overload expressing itself as pulmonary and peripheral oedema
Arrhythmias secondary to changes in potassium and acid-base balance
Features of uraemia – nausea, encephalopathy, drowsiness, confusion, seizures

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8
Q

What are the two types of renal tubular acidosis?

A

Tubular Dysfunction
Renal tubular acidosis – failure of patients to acidify urine in metabolic acidosis.
1. Type 1 or distal RTA – failure to excrete hydrogen ions urine becomes alkaline and blood acidic. Actual problems is failure to reclaim potassium
2. Type 2 RTA or Proximal – affecting proximal tubules resulting in bicarbonate to leak into the urine and so urine becomes alkaline and blood acidic.

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9
Q

How should AKI be diagnosed and investigated?

A

Urine dipstick
U&Es
USS looking for obstruction
CXR – fluid overload

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10
Q

What are the 3 stages of AKI

A

Stage 1 - 1.5-1.9 times baseline creatinine over last week or >26ug/l increase within 48 hours or <0.5ml/kg/h urine output for 6-12 hours

Stage 2 - 2-2.9 times baseline creatinine or <0.5ml/kg/h for > 12 hours

Stage 3 - 3 times baseline creatinine or increase in serum creatinine to 354ug/l or reduction in eGFR to <35ml/min or <0.3ml/kg/h for >24 hours or anuria for >12 hours.

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11
Q

What are the diagnostic criteria for AKI?

A
  1. Rise in serum creatinine of 26umol/l or greater over 48 hours
  2. 50% rise in serum creatinine that has occurred within the last 7 days
  3. Fall in urine output to less than 0.5ml/kg/hour for more than 6 ours in adults and more than 8 hours in children and young people.
  4. 25% or greater fall in eGFR in children and young people within the past 7 days
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12
Q

How should AKI be managed?

A

Assess fluid status
Note if completely anuric check for obstruction especially in catheters
Stop any drugs that reduce kidney function e.g. NSAIDs, ACEi, ARBs, diuretics and aminoglycosides. Also stop metformin, lithium, and digoxin due to increased risk of toxicity

Vasoconstriction of afferent arteriole
Cox-2 inhibitors, Cyclosporine A, NSAIDS, Tacrolimus, Iodinated Contrast

Vasodilation of efferent arteriole
ACEI and ARBs (when used expect 10-20% drop of eGFR but no more)

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13
Q

What are the criteria for referral of an AKI patient to a nephrologist?

A
  • Renal transplant
  • Vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma
  • AKI with no known cause
  • Inadequate response to treatment
  • Complications of AKI
  • Stage 3 AKI
  • CKD stage 4 or 5
  • May require dialysis
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14
Q

What causes calcium and bone problems in CKD?

A

Vitamin D synthesis usually finished in the kidneys, so CKD causes low Vitamin D. Kidneys also secrete phosphate, so CKD causes high phosphate. High phosphate draws calcium out of the bones causing Osteomalacia whilst low vit D causes low calcium. All this in turns results in secondary hyperparathyroidism – brown tumours due to over activity of osteoclasts, this is also known as osteitis fibrosa cystica

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15
Q

What causes anaemia in CKD?

A

Most commonly this occurs due to reduced erythropoietin levels causing a normochromic, normocytic anaemia that becomes apparent when GFR drops below 35ml/min. Can also occur due to reduced absorption of iron, anorexia/nausea, blood loss due to capillary fragility and platelet function

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16
Q

What causes CKD?

A 
Chronic glomerulonephritis
Chronic pyelonephritis
Genetic – PCK, Alport’s
Chronic obstruction
AKI
Hypertension
Cardiovascular disease
Diabetes
Myeloma
Vasculitis and lupus
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17
Q

Why does hypertension occur in CKD?

A

Kidneys detect the low GFR as indicating blood pressure is too low and so attempt to revert this by releasing renin, conserve salt and water and active sympathetic nervous system which all increase blood pressure.

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18
Q

What are the clinical features of CKD?

A 
Itching
Fatigue and malaise due to anaemia
Weigth loss due to poor appetite
Nausea and vomiting
Insomnia
Muslce cramps
Headaches
Erectile dysfunction 
Fluid overload in advanced disease 
Hypertension
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19
Q

How should CKD be investigated?

A

FBC and U&Es – GFR and ACR is (albumin creatinine ratio in the urine) is used to diagnose and classify. ACR sample taken as first-pass morning urine specimen.
Parathyroid function, phosphate, and calcium.
USS looking at size of kidneys and for cysts.
Urine Dipstick
Consider Renal biopsy if appropriate
USS looking at size of kidneys and for cysts.

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20
Q

How is CKD classified based on ACR?

A

A1 – ACR < 3
A2 – ACR 3-30
A3 – ACR > 30

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21
Q

How is CKD classified based on GFR?

A

G1 – GFR > 90 with some signs of kidney damage on other tests
G2 – GFR 60-90 with some signs of kidney damage
G3a – GFR 45-59 – this is a moderate reduction in kidney function
G3b – GFR 30-44 – this is a moderate reduction in kidney function
G4 – GFR 15-29 – this is severe reduction in kidneys function
G5 – GFR < 15 – established kidney failure dialysis or transplant likely required

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22
Q

When should a CKD patient be referred to a nephrologist?

A
  • eGFR < 30
  • eGFR decrease by 25% or 15 or more within 1 year
  • ACR >70mg/mmol unless known to be caused by diabetes and already treated
  • ACR > 30mg/mmol or more with persistent haematuria after excluding UTI
  • Uncontrolled hypertension despite use of at least 4 antihypertensives
  • Suspected or confirmed rare or genetic cause of CKD e.g. PCKD
  • Suspected renal artery stenosis
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23
Q

How should hypertension be managed in CKD?

A

Aim for 140 systolic, key to managing proteinuria are ACEi or ARB. As these drugs reduce filtration pressure a small falling GFR should be expected. NICE suggest 25% reduction in GFR or a rise of up to30% creatinine is acceptable. Furosemide also useful, especially when GFR drops below 45ml/min and has the added benefit of lowering serum potassium.

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24
Q

How are lipid levels managed in CKD?

A

Atorvastatin 20mg should be offered to patients with CKD. Increase the dose of greater than 40% reduction in non-HDL cholesterol not achieved and FR > 30.

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25
How is anaemia managed in CKD?
Target Hb of 100-120g/ml. Check iron levels and correct this first before administering erythropoiesis stimulating agents such as erythropoietin and darbepoetin.
26
What are the side effects of erythropoietin?
``` SE of erythropoietin • Accelerated hypertension which can lead to encephalopathy and seizures • Bone aches • Flu-like symptoms • Allergic reaction • Pure red cell aplasia • Raised PCV increases risk of thrombosis • Iron deficiency ```
27
How are calcium and phosphate managed in CKD?
Vitamin D replacement (calcitriol) for those that need it. Reduce dietary intake of phosphate and use phosphate binders – calcium based binders can cause hypercalcaemia and vascular calcification, non-calcium based binders such as Sevelamer are becoming more popular which binds dietary phosphate and prevents absorption. Parathyroidectomy may be required in some cases
28
If a patient becomes acidotic due to CKD how can this be managed?
Oral bicarbonate supplements to manage acidosis
29
When is renal replacement therapy required in CKD?
This is required in renal failure which is when native renal function declines to a level no Longer adequate to support health. Usually when eGFR 8-10 Ml/Min and there is presence of uraemic symptoms – acidosis, pericarditis, fluid overload and hyperkalaemia.
30
What is haemodialysis and what are the potential complications?
This is the most common and involves regular filtration of blood via a dialysis machine, usually 3 times a week. 8 weeks prior to starting an arteriovenous fistula must be formed. ``` Complications • Site infection • Endocarditis • Stenosis at site • Hypotension • Cardiac arrhythmia • Air embolus • Anaphylactic reaction to sterilising agents • Disequilibration syndrome ```
31
What is peritoneal dialysis and what are the potential complications?
A different form of dialysis where the filtration takes place in the abdomen. High dextrose solution injected via a permanent catheter into the peritoneal space, this draws out waste products from the blood. The fluid is then drained after 4-8 hours or a machine does it automatically overnight. This is termed Continuous peritoneal dialysis (CAPD) which involves four 2L exchanges a day. ``` Complications • Peritonitis • Sclerosing peritonitis • Catheter infection • Catheter blockage • Constipation • Fluid retention • Hyperglycaemia • Hernias • Back pain • Malnutrition ```
32
How does someone receive a kidney transplant and what are the potential complications?
Renal transplant Average wait for a new kidney is 3 years although crossmatched friends and family may be able to speed the process up. Extra kidney inserted in the groin and connected up to the external iliac vessels. Life-long immunosuppressants are required following this. ``` Complications • DVT/PE • Opportunistic infections • Malignancies (particularly lymphoma and skin cancer) • Recurrent of original disease • Urinary tract obstruction • Cardiovascular disease • Graft rejection ```
33
What are the two main categories of polycystic kidney disease?
Autosomal dominant is the most common | Autosomal recessive on Chromosome 6 also exists but rarer – high mortality rate
34
What causes AD PCKD?
usually inherited but can be de novo in 10% of cases 2 main mutations PCKD1 – chromosome 16 end stage renal failure at around 50 accounts of 85% of cases PCKD2 – chromosome 4 end stage renal failure at around 70 accounts for 15% of cases
35
How does PCKD present?
Usually clinically silent unless the cysts become so large they are symptomatic ``` Hypertension Headaches Abdominal pain Flank pain Haematuria Renal calculi Hepatic involvement such as interlobular fibrosis ```
36
What associated symptoms are there with PCKD?
Liver, ovarian and Pancreas Cysts | Berry aneurysms
37
How is PCKD diagnosed and screened for?
USS scan is the gold standard Diagnosis by number of cysts which increase in prevalence with age so need higher number of cysts as you age for diagnosis. Should screen for intracranial aneurysms if less than 65 years and have family history of aneurysms as increased incidence in PCKD Relatives of affected individuals screened with abdominal USS US diagnostic criteria Two cysts unilateral or bilateral at < 30yrs Two cysts in both kidneys at age 30-59yrs Four cysts in both kidneys if aged >60yrs
38
How is PCKD managed?
Selected patients can receive Tolvaptan (vasopressin receptor 2 antagonist) which slows the progression of cyst development and renal insufficiency. Criteria for use: • CKD stage 2 or 3 at presentation • Evidence of rapid progression High fluid intake Treat BP to 130/80 using ACEi, thiazide like diuretics and Beta blockers (do not use calcium channel blockers) Dialysis or transplant
39
What is Rhabdomyolysis?
Breakdown of skeletal muscle causes toxic levels of myoglobin in the blood which is filtered by the kidney where it causes obstruction and inflammation.
40
What are the common causes of Rhabdomyolysis?
``` Crush injuries Strenuous exercise Medications Drug abuse Fall with long lie Epileptic seizures Drugs: Ecstasy and statins (especially when co prescribed with clarithromycin) ```
41
What are the clinical features of Rhabdomyolysis?
AKI and disproportionately high creatinine Raised CK Myoglobinuria (Light brown coloured urine) Confusion due to hypocalcaemia (myoglobin binds to calcium) Elevated phosphate (released from myocytes) Hyperkalaemia Metabolic acidosis
42
How should Rhabdomyolysis be investigated?
U&Es including calcium Creatine kinase and LDH MSU
43
How is rhabdomyolysis managed?
IV fluids Urinary alkalisation Dialysis
44
What is a lower UTI?
Infection of the urethra, bladder or prostate
45
What causes a lower UTI?
E. Coli | Staphylococcus Saprophyticus
46
What are the clinical features of a lower UTI?
``` Dysuria Frequency Urgency Cloudy and offensive smelling urine Lower abdominal pain Low grade fever Malaise Acute confusion in the elderly ```
47
What are the investigations of choice for a lower UTI?
``` Urine dipstick Urine culture (always send a MSU in those aged >65 or with visiblen/non-visible haematuria) ```
48
How should lower UTIs be managed in Non pregnant women, men and catheterised patients?
Non-pregnant women – Trimethoprim or nitrofurantoin for 3-5 days Men – Trimethoprim or nitrofurantoin immediately for 7 days Catheterised – only treat symptomatic infections and treat as for males regardless of gender
49
What is an upper UTI?
Pyelonephritis | Definition – infection of the kidneys or renal pelvis
50
What causes upper UTIs?
Typically, an ascending infection from lower urinary tract E. Coli Staphylococcus Saprophyticus
51
What are the clinical features of an upper UTI?
``` Severe flank and loin pain (loin to groin) Fever and rigors Nausea and vomiting Burning on urination White cell casts in the urine ```
52
How should an upper UTI be investigated?
Urinalysis including dipstick and MSU Routine blood tests USS or CT if suspecting alternate diagnosis or abscess
53
How are upper UTIs managed?
Consider all upper UTIs for admission to hospital Simple Low prevalence of resistance, no high-grade fever systemically well Treat with ciprofloxacin or ceftriaxone or trimethoprim for 10-14 days Complicated High grade fever, systemically unwell Intravenous hydration and more broad-spectrum antibiotics for 10-14 days
54
What screening should diabetic patients have for diabetic nephropathy
All patients should be screened annually using Urinary Albumin: creatinine ratio (ACR) using an early morning specimen. If ACR > 2.5 this suggests microalbuminuria.
55
How should diabetic nephropathy be managed?
``` Dietary protein restriction Tight glycaemic control BP aim for < 130/80 ACEi or ARB independent of blood pressure control Control lipidaemia using statins ```
56
What is contrast media nephrotoxicity?
25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media.
57
What are the risk factors for nephrotoxicity from contrast media?
``` Known renal impairment (especially diabetic nephropathy) Age > 70 Dehydration Cardiac failure Nephrotoxic drugs such as NSAIDs ```
58
How can we prevent nephrotoxicity from contrast media?
Normal saline 1ml/kg/hour for 12 hours pre- and post-procedure.
59
What are the two main causes of renal artery stenosis?
Usually secondary to renal artery atherosclerosis 90% of cases. Can also be due to Fibromuscular dysplasia in which 90% of patients are female.
60
What are the features of renal artery stenosis?
Hypertension Chronic kidney disease or more sensitive to AKI from drugs/dehydration Flash pulmonary oedema
61
What is glomerulonephritis?
Glomerulonephritides present on a spectrum from nephrotic syndromes (proteinuria due to podocyte pathology) to nephritic syndromes (haematuria due to inflammatory damage). Proteinuria is often seen when scarring occurs in the glomerular and so proteinuria often complicates nephritis presentations.
62
What are the baseline requirements before a renal biopsy can take place?
``` BP < 160/95 Hb > 90 Plt > 100 Clotting < 1.2 Stop anticoagulants/antiplatelets (aspirin 1 week, INR < 1.2 and LMWH 1 day) ```
63
What are the common complications of renal biopsies?
Pain – back and loin Visible haematuria Bleeding Requirement for transfusion
64
How should a patient be managed post renal biopsy?
Bed rest for minimum of 4 weeks Monitor BP, pulse, symptoms, and urine colour Do not discharge until visible haematuria settles Restart blood thinners 1 day after
65
What are the clinical features of nephrotic syndrome?
Triad of: 1. Proteinuria (>3g/day) hyperlipidaemia, 2. Hypoalbuminaemia 3. Oedema. Also, loss of clotting factors but also increased risk of DVT/PE due to loss of antithrombin III, hyperlipidaemia, CKD, increased risk of infection due to Ig loss and hypocalcaemia as Vitamin D and binding protein lost.
66
Which conditions cause a nephrotic syndrome?
* Membranous Glomerulonephritis * Focal segmental Glomerulonephritis * Minimal change Disease * Amyloidosis * Diabetic nephropathy
67
What is membranous glomerulonephritis?
Definition – IgG immune complex deposition on podocytes, usually affects people between the ages of 30-50. It is the most common type of glomerulonephritis in adults and 3rd most common cause of end-stage renal failure.
68
What causes membranous glomerulonephritis?
Idiopathic due to anti-phospholipase A2 antibodies Infections such as hepatitis B, malaria, and syphilis Malignancy (prostate, lung, lymphoma, and leukaemia) Drugs such as gold, penicillamine and NSAIDs Autoimmune disease such as systemic lupus erythematous, thyroiditis and rheumatoid.
69
How does membranous glomerulonephritis appear on biopsy?
Renal biopsy and electron microscope demonstrates thickened basement membrane and subepithelial electron deposits creating a ‘spike and dome appearance’. Can check for the anti-phospholipase A2 receptors antibody which is present in 70-80% of idiopathic cases.
70
How is membranous glomerulonephritis managed and what is the prognosis?
Prognosis 1/3 improve 1/3 stay the same 1/3 develop CKD All patients receive ACEi or ARB II to reduce proteinuria If severe or progressive, then immunosuppressive therapy Consider anticoagulation for high risk patients
71
What is focal segmental glomerulosclerosis?
Definition – focal meaning some glomeruli, segmental meaning only parts of the glomerulus and sclerosis meaning scarring. It is the second most common cause of nephrotic syndrome and has a high recurrence rate in renal transplant.
72
What causes focal segmental glomerulosclerosis?
``` Idiopathic Secondarily to renal pathology such as IgA nephropathy and reflux nephropathy HIV Heroin Alport’s syndrome Sickle-cell ```
73
How does focal segmental glomerulosclerosis appear on biopsy?
Kidney biopsy looking for focal and segmental sclerosis and hyalinosis on light microscopy. Effacement of foot processes seen on electron microscopy.
74
How is focal segmental glomerulosclerosis managed?
Steroids and Immunosuppressants However unlike minimal change disease this does not respond well to steroids and usually progresses to chronic kidney failure. ACE inhibitors, ARB, and tight blood pressure control Kidney transplant or dialysis
75
What is minimal change disease?
Definition – loss of podocyte foot processes. Most common in young children but can rarely occur in adults. Having one or more autoimmune disease increases your risk of developing the disease.
76
What causes minimal change disease?
Drugs – NSAIDs and rifampicin Hodgkin’s lymphoma Infectious mononucleosis
77
How does minimal change disease present?
Nephrotic syndrome Hypertension is rare Highly selective proteinuria only losing intermediate sized proteins such as albumin and transferrin.
78
How does minimal change disease appear on biopsy?
Biopsy demonstrates normal glomeruli o light microscopy but on electron microscopy there will be fusion of podocytes and effacement of foot processes.
79
What is the prognosis of minimal change disease and how is it managed?
Prognosis 1/3 have just one episode 1/3 have infrequent relapses 1/3 have frequent relapses which stop before adulthood Majority of cases are steroid responsive but if resistant can use cyclophosphamide
80
What are the clinical features of a nephritic syndrome?
Proteinuria (<3g/day), haematuria, oliguria (less ten 200ml per 24hr), hypertension, occurs abruptly and azotemia (uraemic symptoms).
81
Which conditions cause nephritic syndrome?
* Rapidly Progressive Glomerulonephritis * IgA nephropathy * Alport syndrome * HSP
82
What is rapidly progressive glomerulonephritis?
Definition – rapid loss of renal function associated with formation of epithelial crescents in the majority of glomeruli
83
What are the main causes of rapidly progressive glomerulonephritis?
* Goodpasture’s syndrome (now known as Anti-glomerular basement membrane disease), this is a rare form of small vessel vasculitis caused by anti-glomerular basement membrane antibodies against type IV collagen. It effects the lungs as well as the kidneys. * Wegener’s Granulomatosis – autoimmune condition associated with necrotising granulomatous vasculitis affecting upper and lower airways as well as the kidneys * SLE * Microscopic polyarteritis
84
How does rapidly progressive glomerulonephritis present?
Nephritic syndrome Features specific to the underlying cause Good pasture’s syndrome – haemoptysis Wegener’s – vasculitic rash, sinusitis, epistaxis, dyspnoea, haemoptysis, saddle shaped nose deformity, eye involvement (proptosis) and cranial nerve lesions
85
How should suspected rapidly progressive glomerulonephritis be investigated?
Renal biopsy | Good Pasture’s – Linear IgG deposits along the basement membrane
86
How is rapidly progressive glomerulonephritis managed?
Plasma exchange (ANCA and anti-GBM), steroids, and cyclophosphamide
87
What is IgA nephropathy?
Definition – also known as Berger’s disease is the most common cause of GN worldwide. Classically presents as macroscopic haematuria in young people following a respiratory tract infection. Occurs due to mesangial deposition of IgA immune complexes.
88
What conditions is IgA nephropathy associated with?
Alcoholic cirrhosis Coeliac disease/dermatitis herpetiformis HSP
89
How does IgA nephropathy present?
Nephritic syndrome Commonly young male with nonvisible or episodic visible haematuria Recent respiratory tract infection (12-72 hours of infection) Rarely nephrotic range proteinuria Renal failure rarely occurs. Hypertension
90
How does IgA nephropathy differ from post streptococcal glomerulonephritis?
Associated with low complement levels Main symptoms is proteinuria vs haematuria in IgA nephropathy Typically, in interval between throat or skin infection and presentation
91
How is IgA nephropathy managed?
Steroids and immunosuppressants Manage proteinuria with ACEi or ARB Fish oil if persistent proteinuria
92
What is the prognosis of IgA nephropathy?
Slowly progressive disease with 25% developing ESRF Frank haematuria is a market of good prognosis Being male, large proteinuria >2g/day, hypertension, smoking, hyperlipidaemia are all poor prognostic markets.
93
What is Alport's syndrome?
X-linked dominant disorder (85% of the time, can also be autosomal recessive) of the gene which codes for type IV collagen resulting in abnormal basement membrane.
94
How does Alport's syndrome present?
Failed renal transplant due to anti-GBM antibodies leading to Goodpasture’s type syndrome. Usually presents in childhood. Invisible haematuria and progressive renal failure Bilateral sensorineural hearing loss Lenticonus – protrusion of the lens surface into the anterior chamber Retinitis pigmentosa
95
What investigations should be done in suspected Alport's syndrome?
Renal biopsy – splitting of lamina densa on electron microscopy. Hearing test Molecular genetic testing
96
Which conditions present in a mixed Nephrotic/Nephritic picture?
* Diffuse Proliferative Glomerulonephritis * Membranoproliferative Glomerulonephritis * Post streptococcal Glomerulonephritis
97
What is Diffuse Proliferative Glomerulonephritis?
This is class IV lupus nephritis and is the most common and severe form.
98
How does Diffuse proliferative Glomerulonephritis present on biopsy?
Renal biopsy – glomeruli show a wire loop appearance, thickened capillary wall immune deposits on electron microscopy ad granular appearance on immunofluorescence.
99
How is Diffuse proliferative Glomerulonephritis managed?
Manage hypertension | Corticosteroids an immunosuppressants such as azathioprine/cyclophosphamide
100
What is Membranoproliferative Glomerulonephritis also known as?
Also known as mesangiocapillary glomerulonephritis
101
What are the 3 main types of Membranoproliferative glomerulonephritis?
``` Type 1 (90%) Caused by cryoglobulinemia or hepatitis C Renal biopsy and electron microscopy shows subendothelial and mesangium immune deposits of electron dense material resulting in tram tracking appearance ``` Type 2 (dense deposit disease) Caused by partial lipodystrophy (classically have a loss of subcut tissue from their face and facto H deficiency. Caused by persistent activation of the alternate complement pathway Low circulating C3 levels Renal biopsy and electron microscopy show intramembranous immune complex deposits with dense deposits Type 3 Caused by Hepatitis B and C
102
How is Membranoproliferative glomerulonephritis managed?
Steroids
103
What is post streptococcal glomerulonephritis?
Immune complex IgG, IgM and C3 deposition in the glomeruli, most common in the young
104
How does post streptococcal glomerulonephritis present?
``` Typically occurs 7-14 days following a group A beta-haemolytic strep infection (usually strep pyogenes) in the throat or skin Headache and malaise Visible haematuria Proteinuria that can result in oedema Hypertension Oliguria Low C3 and raised ASO titre ```
105
How does post streptococcal glomerulonephritis appear on biopsy?
Renal biopsy – diffuse proliferative glomerulonephritis, endothelial proliferation with neutrophils, electron microscopy show subepithelial humps due to lumpy immune deposits and immunofluorescence shows granular or starry sky appearance.
106
How is post streptococcal glomerulonephritis managed?
Supportive care and antibiotics to clear the bacteria | Has a good prognosis.
107
When are muddy brown casts seen?
Muddy brown casts on urinalysis are pathognomonic of ATN
108
What is acute interstitial nephritis and what are its causes?
Hypersensitivity reaction within the kidney causing interstitial oedema and inflammation. Causes Drugs such as: Penicillin, rifampicin, NSAIDs, allopurinol and furosemide Systemic disease – SLE, sarcoidosis and Sjogren’s Infection
109
How does acute interstitial nephritis present?
``` Fever, rash and arthralgia Eosinophilia Mild renal impairment Hypertension Sterile pyuria White cell casts ```

Medicine (7 decks)

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