Session 7 Flashcards
What is CKD
A progressive deterioration of renal function over months to years
Features of CKD
Measured by eGFR
Usually irreversible, as renal tissue is replaced by extracellular matrix in response to damage
Deterioration can be slowed with treatment
How do you stage eFGR
Using eGFR or Albuminuria
stages for eGFR staging of CKD
Stages for Albuminuria staging of CKD
Treatments for proteinuria
Gives ace inhibitors or angiotensin receptor blockers
ACI/ARB
How does diabetes lead to hyper filtration
Diabetes = high amounts of glucose reabsorbed, coupled with sodium
Less Na+ in tubule, less Na+ delivered in macula densa, activates RAAS,
renin increases, aldosterone increases, BP increases
Over time causes damage to glomerular capillaries and capillary bed
First clue that diabetes is causing hyperfiltration
micro Albuminuria
How do we manage blood pressure in CKD
Anti-hypertensives
Diuretics
Fluid restriction
Blood pressure targets in CKD
Causes of primary CKD
Causes of secondary CKD
Leading causes of CKD and end stage renal failure
Diabetes mellitis
(Also hypertension)
What is the best way to monitor diabetes control in someone with poorly controlled T2DM and CKD
Fasting plasma glucose
What is HbA1c
Glycosylated Hb
RBC lifespan 120 days so good to assess long term control
When is HbA1c not a good test
Anaemia due to CKD due to not enough EPO
What do we need to correct anaemia related to CKD
EPO (supplements and potentially dialysis)
And Iron
Patient with CKD found to have bilateral crackles on lungs and pitting oedema to shins is indicative of
Fluid overload secondary to CKD
Most appropriate diuretic for fluid overload secondary to CKD
A loop diuretic
That inhibits the Na+ K+ 2Cl- co transporter in LoH
Use bigger doses of loop diuretics in CKD
How does impaired renal function impact calcium homeostasis
impaired mineralisation of bone , increased bone resorption, increased PTH, increased osteoclastic activity and hence bone resorption
Decreased calcium absorption, decreased plasma calcium, stimulation of parathyroid glands leading to hyperplasia
These 2 factors together lead to increased plasma phosphate and decreased phosphate excretion
X ray signs of impaired renal function impacting calcium homeostasis
Non-bone calcification
Ureamia symptoms
Features of RRT
End stage renal failure
Renal replacement therapy
How does haemodialysis work
Haemodialysis pros and cons
Peritoneal dialysis pros and cons
How does peritoneal dialysis work
How does renal transplant work
Regulatory impacts of CKD
RAAS to manage fluid overload
Reabsorption of different electrolytes
Acid base balance
Excretory impacts of CKD
Phosphate and potassium not well excreted
Unable to excrete fluid: become fluid overloaded
Endocrine impacts of CKD
EPO, vit D activation
What is glomerulonephritis GN
Inflammation of glomeruli
Often involves immune system
4 structures in glomerulus that can be damaged
Capillary endothelium
Glomerular basement membrane
Mesangial cells
Podocytes
What is nephrotic vs nephritic syndrome
Main characterises of nephrotic syndrome
Triad of:
- Proteinuria >350mg/mmol (3.6g in 24 hrs)
- Hypoalbuminaemia
- Oedema
usually accompanied by high cholesterol
Other features in nephrotic syndrome
BP often normal (can be low or high)
Creatinine may be normal
Proteinuria > 350mg/mmol alone = nephrotic range proteinuria
Causes of primary renal disease / nephrotic syndrome e
Minimal change disease
membranous glomerulonephritis
Focal segmental glomerulosclerosis FSGS
Causes of secondary renal disease / nephrotic syndrome
Diabetes is most common
What is diabetes nephropathy
Leading cause of end stage renal disease
XS glucose in blood binds to proteins especially at efferent arteriole
Hyaline atherosclerosis obstructs blood flow
Effect of diabetic neuropathy on GFR
Initially increase GFR, over time mesangial cells secrete more
structural matrix.
Thickening of basement membrane, GFR decreases
Treatment of diabetic nephropathy
Control Hypertension, good glycemic control, ACE inhibitors, angiotensin receptor blockers
What is minimal change disease
Most common cause of nephrotic syndrome in children under 6
Impacts podocytes, facial oedema presentation
No significant renal changes are seen under light microscope
Prognosis good in children, variables with adults
What is membranous glomerulonephritis
Subepithelial deposition of immune complexes (antibody-antigen complexes)
Thickening of basement membrane
Albumin can leak out of capillaries
40% adult nephrotic syndrome
Treatment for membranous glomerulonephritis
Immunosuppressants, treatment of underlying cuase
What is Focal segmental glomerulosclerosis FSGS
Podocytes damaged
proteins build up in glomerulus- hyalinosis (glassy)- leading to sclerosis
Causes of FSGS
Primary: idiopathic
Secondary: sickle cell disease, HIV, heroin abuse, kidney hyperperfusion
Treatment for FSGS
Steroids, inconsistent results can lead to chronic renal failure
Broad management of nephrotic syndrome
Nephritic syndrome is characterised by
Haematuria
Reduction in GFR (renal impairment/oliguria)
Hypertension
Other features of nephritic syndrome
- Some proteinuria
- Disruption of endothelium results in inflammatory response and damage to the glomerulus
- Onset may be acute or rapidly progressive (RPGN)
- Rapidly progressive. Crescentic GN - a fulminant form of nephritic syndrome
Common causes of nephritic syndrome
IgA nephropathy (berger’s disease)
Rapidly progressive GN (glomerulonephritis)
Goodpasture’s (anti GMB)
Post-streptococcal GN
Features of IGA nephropathy (Berger’s disease)
Most common primary glomerular disease causing recurrent haematuria
Hypertension and IgA levels raised, deposits in mesangium, sclerosis of damaged segment
Treatment of IGA nephropathy Berger’s disease
Control BP, antihypertensives, steroids
20% will develop advanced CKD
Features and treatment of rapidly progressive glomerulonephritis
Features and treatment of Goodpastures syndrome
Features and treatment of post-streptococcal glomerulonephritis
Management of nephritic syndrome
Overview of differential diagnosis of glomerular diseases
