- fatigue - lethargy - confusion - anorexia - nausea - cramps - restless legs - insomnia - itching

- amenorrhea - hiccough - reduced body temp - weight loss - pericarditis - pleuricy - seizures - encephalopathy

Renal Disease Flashcards by Aarya Sumesh

How does renal disease present (4):

incidental finding
symptomatic
associated with a systemic disorder
inherited disease screening

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Renal Disease: Incidental Finding:

abnormal renal function tests
urinary abnormalities
hypertension
small/dilated kidneys on imaging

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Renal Disease: Asymptomatic Presentation:

kidneys have enormous excess
capacity
GFR<50% before creatinine rises
above normal range
symptoms related to reduced
kidney function unusual until GFR
<15

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Renal Disease: Renal Function Tests:

bloods: Na,K, urea, creatinine, bicarb
(any abnormal)
ABG: pH decreases, lactate???

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Renal Disease: Hyperkalaemia:

mainly intracellular
if kidneys do not excrete potassium
plasma potassium high
disrupts electrochemical gradient
causing cardiac arrythmias/arrest
medical emergency if above 6.5

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Renal Disease: Urine Dipstick:

***blood (non-visible)
***protein
glucose
ketones
billirubin

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Only high molecular weight protein may appear in the urine.

True or False?

False
Low and high molecular weight

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Renal Disease: Measurement of proteinuria:

Urinary protein/creatinine ratio
(PCR)
Urinary albumin/creatinine ratio
(ACR)
ratio avoids 24hr urine collection
PCR/ACR x10=24hr excretion
screening for diabetes, CKD, CVD
albumin testing has become the
standard assay

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Renal Disease: Interpretation of Serum Creatinine and ACR:

proteinuria increases as CKD
progression risk increases
ACR (protein/albumin ratio) <3 =
normal
ACR 3-30 = moderately increased
ACR >30 = severely increased

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Increased proteinuria is associated with faster decline in renal function.

True or False?

True

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Renal disease: Non-visible Haematuria:

urine microscopy vs dipstick
bleeding from kidney:
- red cell cast on microscopy
- indicates glomerular disease
bleeding from lower renal tract:
- renal pelvis and downwards
- tumours/stones
- bladder catheter

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Renal Disease: Symptomatic Presentation:

general malaise
uraemia
nephrotic syndrome
nephritic syndrome
AKI
CKD
visible haematuria
frequence, dysuria
pain

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Uraemia symptoms:

fatigue
lethargy
confusion
anorexia
nausea
cramps
restless legs
insomnia
itching

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Uraemia Signs:

amenorrhea
hiccough
reduced body temp
weight loss
pericarditis
pleuricy
seizures
encephalopathy

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4 signs of renal disease:

peripheral oedema
periorbital oedema
purpura
muddy, brown, foamy, coco cola
urine

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What sign of renal disease is this?

Purpura

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Causes of Renal Disease:

insert slide

1,2, = pre-renal can lead to renal
3, 4 , 5, 6= renal
7,8 = post-renal

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8 Causes of Renal Disease:

1) Pre-Renal AKI
2) Renal Artery/arteriole occlusion
3) Small Vessel Disease
4) Glomerular Disease
5) Acute Tubular Necrosis
6) Acute Interstitial Nephritis
7) Intra-Tubular Obstruction
8) Post-Renal Obstruction

AKIRASVDGDATNAINITOPRO

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Key Features of Normal Glomerulus:

capillaries with fenestrated
epithelium
basement membrane
single layer of podocytes
foot processes
supporting mesangial cells (support
and can contract, decreasing SA for
filtration)

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Podocyte Injury can be due to:

Cytokines
Pressure (hypertensive
glomerulonephropathy)
Immunoglobulin deposition (IgA
Nephropathy)

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Patterns and Causes of Glomerular Disease:

epithelial cell swelling
basement membrane thickening
electron dense deposits
subendothelialy
capillary lumen narrowed
endothelial cell swelling
fused foot process
mesangial matrix deposits
slight proliferation of mesangial cells

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Renal Disease: Renal Biopsy:

renal biopsy gives an accurate
diagnosis:
- patterns of disease on light
microscopy
- patterns of disease on electron
microscopy
- immunoflorescent antibodies

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Examples of Glomerularnephritis:

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Immune Diseases of the glomerulus:
Type 1
Type 2
Type 3
Type 4

type 1: IgE: no known renal disease
type 2: IgG, IgM: membranous
glomerularnephritis
type 3: immune complexus: Hep B,C
type 4: T cells: Sarcoid, sclerosis

Immune Disease of the Glomerulus: What types of mediation?

- antibody mediated - antigen/antibody complex mediated

Immune Disease of the Glomerulus: Antibody mediated:

- antibodies directly bind to cell - causes damage through the activation of complement system - activates apoptosis

Immune Disease of the Glomerulus: Antigen/antibody complex mediated:

- immune complexes form in circulation elsewhere and get trapped in glomeruli - effects depend on location of deposition within the glomerulus

Crescentic glomerulonephritis

accumulation of WBC and proliferated parietal cells crescents compress the capillary tufut associated with severe disease histological finding

Diffuse Proliferative Glomerulonephritis

- poststreptococcal sore throat - increased cells in the glomerulus - capillaries occluded by inflammatory cells - sparse deposits of IgG immune complexes along capillary loops

Membranous glomerulonephritis

- diffusely thickened basement membranes - granular despoitis of IgG immune complexes across peripheral glomerular capillary walls

Small Vessel Disease: - vasculitis - thrombosis - atherosclerosis

- inflammation of the vessels - blockage due to blood clot - narrowing due to hypertension or diabetes

Hypertensive nephropathy leads to glomerulosclerosis

insert slide

Clinical Features of hypertensive nephropathy:

- blacks>caucasians - chronic hypertension - 2nd commonest cause of end stage renal disease - haematuria - visible proteinuria

Treatment of Hypertensive Nephropathy:

- antihypertensives (ACE inhibitor) aiming for 130/80

Biopsy finding of hypertensive nephropathy:

- LM: glomerular sclerosis, tubular atrophy, arteriosclerosis - IHC: no immune deposits

Diabetic Glomerulonephropathy

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Diabetic Nephropathy: Clinical Features:

- increasing albuminuria before overt kidney disease - often presents with nephrotic syndrome

Diabetic Nephropathy: Biopsy findings:

rarely done nodular glomerulosclerosis

Diabetic Nephropathy:

- BP control - reduce proteinuria with ACE inhibitors - diabetic control

Nephrotic Syndrome:

- a triad of: - proteinuria - low albumin - oedema - associated features: - high cholesterol - tendency to thrombosis - tachycardia - oedema that begins in the face - pale skin fissures - vomiting

Pathophysiology of Nephritic and Nephrotic Syndromes

insert slide

Comparison of Nephritic and Nephrotic Syndromes:

insert

Acute Tubular Necrosis Pathophysiology (4):

- Induction: - initial event (afferent arteriole constriction) - reduced GFR - Extension: - ongoing hypoxia - inflammatory response - corticomedullary nephrons most affected - necrosis and cell death - Maintenance: - restoration of blood flow - reversal of hypoxia - cellular repair and proliferation - Repair: - restoration of tubular integrity - improvement in renal function

What is interstitial nephritis?

inflammation within the mesangium of the kidney

4 indications for urgent renal replacement therapy:

- uncontrollable fluid overload - uncontrollable, severe metabolic acidosis - uncontrollable hyperkaelaemia - uraemic pericarditis/ encephalopathy

Acute or Chronic Renal Failure?

Acute: - acidotic, unwell - normal Ca2+ - normal size kidneys Chronic: - surprisingly well - low Ca2+/ renal osteodystrophy - small kidneys - pigmented

What is involved in Renal Replacement Therapy?

- haemodialysis - peritoneal dialysis - renal transplant

Renal Replacement Therapy: Haemodialysis:

- vascular acess - 3-4hrs 3x a week - restrictive eg holidays

Renal Replacement Therapy: Peritoneal Dialysis:

- peritoneum used as dialysis membrane - electrolytes and toxins move down conc grad - 4-5 exchanges per day - no machine - infection is complication

Renal Replacement Therapy: Kidney Transplantation:

- live donor - cadavaric donor - original kidneys left behind - usually left kidney behind right iliac fossa

Maximum Conservative Tratment:

- low Na+/K+ diet - low sugar intake - no smoking - ACE inhibitor for hypertension - control of diabetes and cholesterol

Cystic Renal Disease:

- autosomal dominant polycystic kidney disease - recessive as well - simple cysts - cystic dysplastic: congenital, unilateral malformation - hydronephrosis: mistaken for cysts

ADPKD

- autosomal dominant polycystic kidney disease - autosomal dominant mutation in PKD1, chromosome 16, encodes for polycystin 1 protein in cilia - progressive increase in size, no. cysts - gradual decline in renal function - asymptomatic till 30-40 - presents with renal insufficiency, haematuria and hypertension - abdominal mass and flank pain - end stage renal failure in 70s

ARPKD:

- autosomal recessive polycystic disease - multiple small cysts in renal cortex and medulla - multiple liver cysts, hepatic fibrosis - associated with pulmonary hypoplasia - presents in infancy with progressive often fatal renal failure

Simple Renal Cysts:

- acquired cysts - simple (water density, thin wall, no nodules) - differentiate from cystic cancers