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Kidneys Flashcards

1
Q

What is the pathophysiology of Alport’s Syndrome?

A

It is an X-linked genetic disease and therefore seen in males

There is a defect in the ALPHA CHAIN of TYPE 4 COLLAGEN

This collagen is present in 2 main regions- The Glomerular Basement Membrane and the Eyes and Ears (Cochlea, Retina and Cornea)

So there would be haematuria, proteinuria AND hearing/ visual loss or defects

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2
Q

What are the 5 signs of Nephritic Syndrome seen in Alport’s Syndrome?

What are the visual, auditory and behavioural symptoms also seen in Alport’s Syndrome

A

Proteinuria

Microscopic or gross haematuria

Hypertension

A PERIPHERAL oedema

Fatigue and Dyspnoea

Opthalmological- Cataracts, Corneal Dystrophy, Lenticonus (the lens protrude into the anterior chamber)

Auditory- Sensorineural Hearing Loss

Behavioural- Learning disability

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3
Q

What 5 investigations should be conducted if Alport’s Syndrome is suspected?

A

Assess for Sensorineural Hearing Loss

Urinalysis- check for Proteinuria and Haematuria

U&Es- Check for signs of Renal Failure- High Creatinine and Low eGFR

Renal Ultrasound to exclude structural abnormalities

Renal Biopsy- when viewed under Electron Microscopy, you’d see the Longitudinal Splitting of the Lamina Densa with short stubs of Fibrils- forming a BASKET WEAVE APPEARANCE

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4
Q

What is the 2 step management plan for Alport’s Syndrome?

Why may transplantation fail?

A

ACE inhibitor- used as a Renoprotective drug if Haematuria or Proteinuria is present

Renal Replacement Therapy- Dialysis and Transplantation may be needed in an advanced disease

But- after transplantation, transplant failure may occur due to the presence of Anti-GBM Antibodies- which results in a clinical picture similar to Goodpasture’s Syndrome

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5
Q

What determines whether a patient has Chronic Kidney Disease?

A

If there are abnormalities in either the kidney structure or function occuring for more than 3 months

Or any marker of kidney injury, or a GFR<60 measured on 3 different occasions- separated by at least 90 days

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6
Q

What are the 2 most common causes of Chronic Kidney Disease?

A

Diabetes and Hypertension

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7
Q

Chronic Kidney Disease can result in Glomerular Scarring- what are the 3 things this can typically result in?

A

Metabolic derangement- due to HYPERKALAEMIA and URAEMIA

Anaemia- due to the reduced ERYTHROPOEITIN

CKD Mineral Bone Disease

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8
Q

Why is Chronic Kidney Disease a risk factor for Cardiovascular Health?

A

It results in Hypertension, Hypercholesterolaemia and Heart Failure

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9
Q

What are the 7 risk factors for Chronic Kidney Disease?

A

Age>50

Afro-Caribbean

Diabetes

Hypertension

Glomerular Nephritis

Nephrotoxic Drugs (such as NSAIDs)

Enlarged PROSTATE

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10
Q

What are the 8 signs of Chronic Kidney Disease?

A

Lethargy

Pruritus

Frothy Urine

Swollen Ankles (Peripheral Oedema)

Fluid Overload

Hypertension

Anorexia

Uraemic Sallow (yellow or pale brown skin colour)

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11
Q

What 7 investigations are to be considered in Chronic Kidney Disease?

A

Urine Dip for Proteinuria and Haematuria

Work out the Urine Albumin:Creatine Ratio (a ratio that is 3 or above suggests Proteinuria)

FBC- Normocytic Normochromic Anaemia- due to the reduced Erythropoeitin

Bone Profile and PTH- The patient is at risk of (3)- Hypocalcaemia, Hyperphosphataemia and Secondary or Tertiary Hyperparathyroidism

Renal Ultrasound- Bilateral Kidney Atrophy can be seen

CT scan if an obstructive cause is suspected

Renal biopsy if an intrarenal cause is suspected- such as Nephritic or Nephrotic Syndrome

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12
Q

What is the 6 step management plan for Chronic Kidney Disease

A

Stop SMOKING

Avoid Nephrotoxic Drugs (such as NSAIDs)

Have a low salt/ potassium diet with FLUID RESTRICTION

Manage the Cardiovascular Risk Factors (2)

  • Hypertension- Give an ACE Inhibitor (first line) if the AC Ratio is raised (a sign of proteinuria). But stop if Creatinine rises higher than 30% or if the eGFR falls more than 25%. If AC ratio is not raised- then normal Hypertension management
  • Hypercholesterolaemia- Give a Statin- Like Atorvastatin

Anaemia- target 10-12 Hb

  • Iron Replacement
  • Then Erythropoeisis Stimulating Agents (such as Erythropoeitin or Darbepoetin)

Renal Replacement Therapy (if eGFR<10 or if there are signs of Uraemia)
- Dialysis then Renal Transplant

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13
Q

What are the 7 Complcations of Chronic Kidney Disease?

A

Heart Failure- due to the Fluid Overload and the Anaemia

Chronic Kidney Disease- Mineral Bone Disease

Secondary and Tertiary Hyperparathyroidism

Anaemia- Normocytic Normochromic

Hyperkalaemia

Uraemia

Metabolic ACIDOSIS

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14
Q

What is CKD mineral bone disease?

A

A bone disease which occurs in patients with Chronic Kidney Disease

It is characterised by the widespread bone pain

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15
Q

What 3 metabolic changes does CKD Mineral Bone Disease result in?

A

Reduced 1-Alpha Hydroxylase activity leads to REDUCED VITAMIN D ACTIVATION

Reduced renal excretion of Phosphate results in HYPERPHOSPHATAEMIA. This stimulates bone resorption and leads to OSTEOMALACIA

HYPOCALCAEMIA

The Low Calcium, High Phosphate and Low Vitamin D leads to Secondary Hyperparathyroidism

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16
Q

What 5 bone conditions can CKD Mineral Bone Disease manifest as?

A

Osteoporosis

Osteosclerosis

Osteomalacia (due to the low VITAMIN D)

Osteitis Fibrosa Cystica- The Hyperparathyroid Bone Disease

Adynamic Bone Disease- due to the reduction in Osteoblast and Osteoclast activity

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17
Q

What are the 4 metabolic changes seen in the bloods of Secondary Hyperparathyroidism

A

LOW or NORMAL CALCIUM
HIGH or NORMAL PHOSPHATE
LOW VITAMIN D

HIGH PTH

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18
Q

What are the 4 signs of CKD Mineral Bone Disease?

A

Asymptomatic in early stages

Bone and Joint Pain

Bone Fractures and Deformation

Reduced Mobility

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19
Q

What are the 5 investigations to be ordered if Chronic Kidney Disease Mineral Bone Disease is suspected (if eGFR is less than 30 in a patient with bone pain)?

A

Hypocalcaemia

Hyperphosphataemia

Low Vitamin D

Secondary or Tertiary Hyperparathyroidism

Measure their eGFR

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20
Q

What is the aim and 5 step management plan for CKD Mineral Bone Disease?

A

The Aim is to reduce the levels of SERUM PHOSPHATE and PTH

First line- Reduce DIETARY PHOSPHATE- reduce MEAT and FISH and NUTS/ BEANS and DAIRY PRODUCTS

Vitamin D Replacement- as the 1-Alpha Hydroxylase Enzyme is still functioning. Give CHOLECALCIFEROL. In Later Stages, give ALFACALCIDOL or CALCITROL

Give Phosphate-Binders to tackle the high phosphate levels.

  • Calcium-based phosphate binders can be used (CALCIUM ACETATE is first line) but can result in VASCULAR CALCIFICATION and HYPERCALCAEMIA.
  • Non-calcium-based phosphate binders can be used if the calcium-based binders are ineffective- such as SEVELAMER, LANTHANUM and ALUMINIUM (Sevelamer also tackles HYPERCHOLESTEROLAEMIA)

Bisphosphonates given to Prevent and Treat Osteoporosis if eGFR<30

Parathyroidectomy in Tertiary Hyperparathyroidism

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21
Q

What us the pathophysiology of IgA Nephropathy

A

It is the deposition of IgA immune complexes in the MESANGIUM of the GLOMERULUS- which results in nephritic syndrome and end-stage kidney failure

Deposition in the MESANGIUM results in MESANGIUM PROLIFERATIVE GLOMERULONEPHRITIS due to TYPE 3 HYPERSENSITIVITY

This activates the ALTERNATIVE COMPLEMENT PATHWAY- C3 is converted to C3a and C3b which triggers glomerular injury

(This has a significant overlap with Henoch-Schonlein Purpura)

This typically happens after an infection of the mucosal lining- such as a URTI or Gastroenteritis

22
Q

What are the 2 main risk factors for IgA Nephropathy?

A

Having a URTI or Gastroenteritis

23
Q

What are the 7 signs of IgA Nephropathy

A

Very similar to Post-streptococcal Glomerulonephritis

  • Haematuria- macroscopic in younger patients and microscopic in older patients
  • Foamy urine- proteinuria
  • Pink, red, coke urine- haematuria
  • Sore Throat- Sign of URTI
  • Loose stools and abdominal pain- Gastroenteritis
  • OEDEMA due to PROTEINURIA
  • Cervical Lymphadenopathy suggests URTI
24
Q

What 4 investigations should be ordered if IgA Nephropathy is suspected?

A

Proteinuria and Haematuria

U&Es- baseline renal function to be measured as well as the deterioration

C3 and C4- C4 levels will be normal (C4 is associated with the Classic Complement Pathway)- C3 may be normal or low

Renal biopsy- Mesangial Hypercellularity with positive immunofluorescence for IgA and C3

25
Q

What are the 4 steps for IgA Nephropathy Management?

A

Statins

ACE Inhibitor/ ARB- offer it immediately if Protein:Creatine ratio>100

Corticosteroids- if Proteinuria continues despite the ARB/ACE Inhibitor

Omega 3 Fatty Acids- Offer with the Corticosteroids

26
Q

What organism causes Post-streptococcal Glomerulonephritis?

A

Strep Pyogenes

27
Q

What are the differences between IgA Nephropathy and Post-streptococcal Glomerulonephritis?

A

IgA Nephropathy occurs 1-2 days after URTI/ Gastroenteritis
Post-streptococcal Glomerulonephritis occurs 1-2 weeks after URTI/ Pharyngitis/ Skin Infections

IgA Nephropathy- C3 levels are normal or reduced
Post-streptococcal Glomerulonephritis- C3 and CH50 levels are always reduced

IgA Nephropathy- Mesangial IgA deposits on Renal Biopsy
Post-streptococcal Glomerulonephritis- Positive Streptozyme test

IgA Nephropathy- ACE Inhibitor/ ARB for treatment
Post-streptococcal Glomerulonephritis- Furosemide for treatment

28
Q

What is the pathophysiology of Lupus Nephritis?

What is the most common form of Lupus Nephritis?

A

It occurs in patients with SLE and involves the deposition of antigen-antibody complexes in the kidney

The most common form of Lupus Nephritis is Diffuse Proliferative Glomerulonephritis which presents with Nephritic Syndrome

29
Q

What are the 6 main classes of Lupus Nephritis? And 2 facts about each

A

Class 1- Minimal Mesangial
- Normal renal function. Mild or Incidental

Class 2- Mesangial Proliferative

  • Microscopic HAEMATURIA (with or without PROTEINURIA)
  • Hypertension and Nephrotic Syndrome are rare here
  • Typically responds to Steroids

Class 3- Focal Segmental

  • Usually Nephrotic Syndrome
  • Typically responds to high-dose Steroids

Class 4- Diffuse Proliferative (Most Common)

  • Nephritic Syndrome
  • Treated with Steroids and IMMUNOSUPPRESSANTS

Class 5- Diffuse Membranous

  • Nephrotic Syndrome- Extreme Oedema
  • May have hypertension

Class 6- Sclerosing
- Slowly progressing Renal Failure and Proteinuria

30
Q

What are the 4 investigations to be ordered if Lupus Nephritis is suspected?

A

RENAL BIOPSY- GOLD STANDARD

Check for signs of SLE

Haematuria and Proteinuria in Urinalysis

Reduced eGFR

31
Q

What are the findings on Biopsy for Light Microscopy (5), Electron Microscopy (1) and Immunofluorescence (1) for Diffuse Proliferative Glomerulonephritis (most common form of Lupus Nephritis)?

A

Light Microscopy-

  • Hypercellular glomerulus
  • Thickened basement membrane
  • Endothelial and Mesangial Proliferation
  • Wire-loop appearance
  • Capillary wall thickening in SEVERE DISEASE

Electron Microscopy- Subendothelial IMMUNE COMPLEX DEPOSITION

Immunofluorescence- Granular Appearance

32
Q

What is the 5 step management for Lupus Nephritis?

A

Corticosteroids

Immunosuppressive Agents

  • Cyclophosphamide
  • Azathioprine

Hydroxychloroquine

Renal Replacement Therapy if eGFR continues to deteriorate (Dialysis or Transplant)

ACE Inhibitor preferred in patients with Hypertension and Renal Disease

33
Q

What is the pathophysiology of Membranoproliferative Glomerulonephritis?

A

It involves Mesangial Cell proliferation and Thickening of Glomerular Capillaries

34
Q

What are the 3 types of Membranoproliferative Glomerulonephritis?
What 5 conditions is Type 1 associated with?

A

Type 1 (Most Common)- Associated with (5)-

  • SLE
  • Hepatitis B and C
  • Chronic Lymphocytic Leukaemia
  • Lymphoma
  • Cryoglobulinaemia

Type 2 (Dense Deposit Disease)

  • Activation of the Alternative Complement Pasthwya and therefore LOW levels of C3
  • Associated with (2)- Factor H Deficiency and Partial Lipodystrophy

Type 3-

  • Subendothelial and subepithelial deposits
  • Associated with (2)- Hepatitis B and C
  • ALL of them have LOW C3 levels (HYPOCOMPLEMENTAEMIA) and Mesangial Cell Proliferation
35
Q

What are the 3 main risk factors for Membranoproliferative Glomerulonephritis?

A

Infections- HIV/ Hepatitis B and C/ Endocarditis

Chronic Lymphocytic Leukaemia/ Cryoglobulinaemia

Acquired Partial Lipodystrophy- loss of Fat- Associated with Type 2 Membranoproliferative Glomerulonephritis

36
Q

What are the 4 signs of Membranoproliferative Glomerulonephritis?

A

Foamy Urine (Proteinuria)

Pink, Red or Coke tinged urine (Haematuria)

Oedema (due to Hypogammaglobuminaemia)

Oliguria (<0.5)

37
Q

What 4 things are observed in Renal Biopsy for Membranoproliferative Glomerulonephritis?

A

PAS Staining on Light Microscopy shows Mesangial Cell Proliferation and Capillary Thickening

Type 1- Subendothelial and mesangial immune deposits result in Tram Track Appearance

Type 2- Intramembranous immune complex deposits with Dense Deposits

Immunofluorescence reveals C3 deposition

38
Q

What 4 investigations are conducted in Membranoproliferative Glomerulonephritis?

A

Most children with Nephrotic Syndrome have Minimal Change Disease which would not show up on Renal Biopsy- so treat them with the treatment for MCD which is CORTICOSTEROIDS before the renal biopsy

  • Haematuria and Proteinuria
  • Type 1- Low C3 and C4 is Low or Normal
  • Type 2- Low C3 and C4 is Normal
  • Renal Biopsy is the definitive diagnosis
39
Q

What is the 2 step approach to treating Primary Membranoproliferative Glomerulonephritis and 3 steps for treating Membranoproliferative Glomerulonephritis in general?

A

Primary Membranoproliferative Glomerulonephritis-

  • Oral Cyclophosphamide
  • Oral Mycophenolate Mofentil and Oral Corticosteroids

General-

  • ACE Inhibitor/ ARB offered to all patients with Proteinuria generally
  • Statins are offered to all patients with Nephrotic Syndrome after they are evaluated for having Dyslipidaemia
  • Oral Warfarin- check their Serum Albumin. Patients with low Serum Albumin are at a higher risk of thrombosis
40
Q

What are the three main symptoms of Nephritic Syndrome and Nephrotic Syndrome?

A

Nephritic-

  • Haematuria (mainly)
  • Hypertension
  • Oedema

Nephrotic-

  • Proteinuria (mainly)>3.5
  • Hypoalbuminaemia<30
  • Oedema

(may not always have hypertension)

41
Q

What are the 4 main causes of Nephritic Syndrome?

A

Post-streptococcal Glomerulonephritis

Alport’s Syndrome

IgA Nephropathy

Rapidly-Progressive Glomerulonephritis

42
Q

What are the 5 main causes of Nephrotic Syndrome?

A

Minimal Change Disease

Membranous Glomerulonephritis

Focal Segmental Glomerulosclerosis

Amyloidosis

Diabetic Nephropathy

43
Q

What 2 conditions cause both Nephrotic or Nephritic Syndrome?

A

Diffuse Proliferative Glomerulonephritis

Membranoproliferative Glomerulonephritis

44
Q

What are the 5 main investigations that show signs of Nephrotic Syndrome?

A

Proteinuria >3.5

Hypoalbuminaemia<30- which causes an OEDEMA

Hyperlipidaemia- liver increases synthesis of lipids in response to Low Albumin

Hypogammaglobuminaemia- due to loss of Immunoglobulins in the urine

Hypercoagulability- due to loss of Antithrombin 3, Protein C and S

45
Q

What are the Light Microscopy Findings for Minimal Change Disease, Focal Segmental Glomerulosclerosis, Membranous Nephropathy, Diabetes and Amyloidosis?

A

Minimal Change Disease- Normal glomeruli

Focal Segmental Glomerulosclerosis- Focal and Segmental Glomerulosclerosis

Membranous Nephropathy- Thick Glomerular Basement Membrane

Diabetes- Mesangial Sclerosis and Kimmelstiel-Wilson Nodules

Amyloidosis- Apple-green Birefringence under Polarised Microscopy with Congo Red Stain

46
Q

What are the Electron Microscopy Findings for Minimal Change Disease, Focal Segmental Glomerulosclerosis, Membranous Nephropathy and Membranoproliferative Glomerulonephritis?

A

Minimal Change Disease- Effacement of Foot Processes

Focal Segmental Glomerulosclerosis- Effacement of Foot Processes

Membranous Nephropathy- Subepithelial Immune Complex Deposition

Membranoproliferative Glomerulonephritis-

  • Type 1- Subendothelial Immune Complex Deposition
  • Type 2- Intramembranous Immune Complex Deposition
47
Q

What is the most common cause of Nephrotic Syndrome in children, adults and the elderly respectively? And what diseases are they associated with (1, 4, 4) ?

A

Minimal Change Disease in children
- Hodgkin’s Lymphoma

Focal Segmental Glomerulosclerosis in adults

  • HIV
  • Heroin
  • SLE
  • Sickle Cell Anaemia

Membranous Nephropathy in elderly

  • Malignancy
  • Hepatitis B
  • NSAIDs
  • SLE
48
Q

What are the three types of Rapid Progressive Glomerulonephritis caused by?

A

Type 1- Autoantibodies (Anti-GBM antibodies)

Type 2- Immune Complexes
- Such as from (3)- SLE, IgA Nephropathy, Henoch Schonlein Purpura

Type 3- ANCA-associated Vasculitides

49
Q

What is the presentation for Rapid Progressive Glomerulonephritis?

A

Nephritic Syndrome (Haematuria with Red Cell Casts, Proteinuria, Hypertension and Oliguria)

50
Q

What features of the underlying cause of Rapid Progressive Glomerulonephritis should be looked out for? (2)

A

Anti-GBM disease- Goodpasture’s
- Associated with Haemoptysis

Granulomatosis with Polyangiitis (Wegener’s) presents with a Vasculitis Rash or Sinusitis

51
Q

How do you treat Rapid Progressive Glomerulonephritis?

A

Steroids and Cyclophosphamides

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