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Progressive loss of kidney function over time.
- Decline of kidney function > months
- Evidence of kidney damage (e.g. albuminuria, abnormal biopsy) OR GFR <60 mL/min/1.73m2 (Albuminuria: ACR: 17 mg/g (women) and 25 mg/g (men))

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Patient had aneamia due to decreased production of erythopoeitin

Hypercalcemia

Hyperkalemia

Dyslipidemia - less lypoproteins

Uremic syndrome - (FIND DEFINITION) build op of toxic substances. Characteristics: confusion, nuasea

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PTH was very high in our patient
Calcium was very low

Kidney disease causes both CVD and bone disease

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●       Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)

●       Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)

●       Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2)

●       Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)

●       Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis)

Stage 1&2 are often asymptomatic

If treated on time then it is reversible

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Most common:
Diabetic nephropathy
Glomerulonephritis
Hypertensive nephropathy
Obstructive uropathy
Use of drugs (also herbs in Chinese tea)

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1. In CKD many nephrons have failed and scarred → less nephrons are incharge of filtration

2. Functioning (remnant) nephrons have increased flow per nephron (hyperfiltration) bc renal blood flow is unchanged → adapt with glomerular hypertrophy and reduced arteriolar resistance

3. Increased flow, pressure and shear stress set in motion vicious cycle of raised intraglomerular capillary pressure and strain → accelerate remnant nephron failure

4. Increased flow and strain can be detected as new/increasing proteinuria

- Increased intrarenal activity of RAAS contributes to initial compensatory hyperfiltration and the later maladaptive hypertrophy and sclerosis

- Angiotensin II effects:

- Vasoconstriction efferent arterioles → increasing glomerular hydraulic pressure and filtration fraction

- Upregulate TGF-B (= potent fibrogenic cytokine) → increase collagen synthesis and epithelial cell transdifferentiation to myofibroblasts that contribute to excessive matrix formation

- Upregulate plasminogen activator inhibitor (PAI-1) → inhibits matrix proteolysis by plasmin → accumulation excessive matric and scarring in glomeruli and interstitium

- Albumin can appear in urine carrying bound fatty acids, growth factors, and cytokines

- When reabsorbed in proximal tubule and degraded → can cause proximal tubular cell activation and interstitial scarring

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Left: Healthy

Right: Fibrosis

The round shapes in the left image are the glomeruli, which are thick and damaged on the right side due to fibrosis

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Diabetes affects glomeruli by thickening of the basement membrane and glomerulosclerosis.

Sclerosis means that parts get white

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Everything blue is pathophysiology

- Diabetes mellitus causes kidney hypertrophy and Glomerular hyperfiltration

- Early → microalbuminuria (30-300 mg/24h)

- 7-10 years after type 1 diabetes diagnosis

- Can be detected by calculating albumin/creatinine ratio ACR

- Men → >2.5 mg/mmol

- Women → >3.5 mg/mmol

- Glomerular hyperfiltration

- Mainly bc Afferent arteriole dilation due to:

- Hyperglycemia and high insulin-like growth factor 1 (IGF-1)

- Hyperfiltration of glucose leads to augmented sodium-glucose transport in the proximal convoluted tubule causing enhanced sodium transport

- Cause expansion of blood volume which leads to a rise in GFR

- The rise in proximal reabsorption also leads to a reduced distal fluid delivery which activates the tubuloglomerular feedback with the RAAS system which works to raise the GFR as well.

- Hyperglycemia and AGE

- Hyperglycemia and AGE directly induce mesangial matrix production, cellular expansion and apoptosis.

- The two have also been shown to increase basement membrane permeability to albumin.

- Cytokines

- Elevations in vascular endothelial growth factor (VEGF), transforming growth factor beta (TFG-β), and profibrotic proteins increase damage to the nephrons at different levels; specific mechanisms are unclear.

Main Problems:
- Podocyte loss
- Scarring
- Mesangial damage

Sheer stress - stretch stress

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eGFR
- Only valid if serum creatinine is not falling or rising over days (Steady state)

- Peak GFR abt 120 mL/min/1.73m2

- Mean decline in the third decade of life is abt 1 mL/min/1.73m2 per year

- 70 mL/min/1.73m2 by 70 y/o

higher in men and African population

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Get rid of the toxins in the blood

Avoid nephrotoxic drugs

Dialysis (very important, see figures below for better explanation)
- Hemodialysis: Taking all the solutes out of your system and returning it to your body
- Hemofiltration: Taking it all out and reinjecting with a replacement solution
- Peritoneal dialysis: you can do at home
- Start dialysis at stage 5, first try medication, but once a patient reaches renal failure dialysis is necessary. GFR<10 mark for dialysis

Find guidelines for dialysis

Drugs:
- NSAIDS
- tetracyclines
- ARBs

Transplant
- Higher survival (10 more years)
- Better quality of life
- Blood group compatibility is preferred
- Corrects anemia and red blood cell infertility
- Risks: Rejection, surgical complications

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First image you still see a lot of individual cells
In the last image you see a fibrotic bulk

Main thing to see is that the archtecture is damaged (less cells, thicker, more white)

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Higher risk of infection

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Measure deapth and rebound time of oedema

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Depending on amount of proteins in urine

Normal range 10-20 mg/ml
1+ 30
2+ 40

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Form of osmotic pressure induced by the proteins, mainly albumin, in a blood vessels plasma that causes a pull on fluid back into the capillary.

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Transplant has the highest prognosis of 5-10 years.

Dialysis is a big change in a patients life, lower quality of life