Elevated blood pressure leads to hypertrophic responses in large and small vasculature. Can lead to long-term glomerular damage, although it is compensatory at first. All leads to nephron and tubular damage, which leads to decreases in kidney function. Nephritis leads to the atrophy of tubules. chronical hypertension leads to nephrons loss and function.

Glomerular hyperfiltration and hyperglycemia leads to diabetic nephropathy, glomerular sclerosis and eventually nephron loss.

See table below

There is uremic puritis as a complication of CKD: buildup of phosphate, calcium or PTH. In this patient it was high phosphataemia and PTH.

- What is causing the lethargy and vomiting?

Can be a complication of anemia. Vomiting is due to effects on GI tract.

Look whether there is blood or proteins in urine. Which would suggest if there is a present glomerular disease or not. 

24 hour urinalysis would suggest the urinary production per day as a function of fluid intake per day. The patient case had normal output, but had a leakage of protein over 24h (6-fold the normal protein levels)

White cells (pyuria) can indicate UTI, eosinophiluria (allergic nephritis), casts which form from abnormal cells in tubular lumen, red cell casts which can suggest glomerular nephritis. RBCs can come anywhere from glomerulus to urethra.  

Measure of urinary electrolytes, Urinary Na+ can be useful. Urine osmolality indicated the kidney concentration ability. 

Low urine osmolality normal with high fluid intake, abnormal when the body must concentrate urine (i.e. hypovolemia). 

Urine electrophoresis and immunofixation → necessary for detection of light chains, which can be present without detectable serum paraprotein

Related to the kidney function loss of erythropoetin (defficiency). There are also Fe, Vit. C, RBC destrcution, blood loss etc. 

 Refers to bone mineral disorder and embraces various forms of bone disease that can develop independently or along with CKD, hyperparathyroid bone disease, osteomalacia, osteoporosis, osteosclerosis and adynamic bone disease. 

Pruritus is common in severe CKD and is mainly due to retention of nitrogenous waste products of protein catabolism

Systemic fibrosis disorder, primarily involving skin. Moderate to severe CKD patients and patients on dialysis. Caused with certain contrast agents. 

Decreased gastric emptying, increased reflux, increased risk of peptic ulcers. 
- common in patients with continuous ambulatory peritoneal dialysis. 

Insulin is catabolized by kidneys --> insulin requirements in diabetic patients decrease and CKD progresses. In advanced CKD, patients become more resistant to insulin. 

Lipid abnormalities are very common in CKD patients. Can lead to complications in ESKD. 

Hypoprolactinin anaemia, galacturea, increased LH, decreased testosterone, erectile dysfunction and decreased spermatogenesis. CKD can have negative effects on hormones at systemic levels. 

Uremia disrupts normal muscle energy metabolism. 

CNS: severe uremia can cause depressed cereb function and increased seizure. Can lead to dialysis dementia as progressive neurogenic degeneration occurs. There is also onset of psychiatric signs.

Autonomic NS: impaired afferent vagal function, overactive symp. system (HT), improve after dialysis and transplantation.

PNS: median nerve compression and carpal tunnel syndrome. Polyneuropathy when patients inadequately dialysed. 

Rare complication that is commonly seen in CKD patients (has poor prognosis). Contributes to death of dialysis patients. Presents as painful non-healing eschars (superficial wounds in non-motile patients), dermal necrosis. Histology suggests calcification of vascular system and small vessel thrombosis. 

Life expectancy of CKD patients remains severely reduced compared to normal population due to increased incidence (16-fold) of CV disease, particularly MI, cardiac failure, sudden cardiac death and stroke. 

Uremic pericarditis: a feature of pre-terminal uremia or inadequate treatment. Atrial arrythmias, pericardial tamponade.

Dialysis pericarditis: can be cause by surgery in a patient when  they are receiving adequate dialysis. 

ADPKD

Drug approach to renonephroapthies. Goals are to manage HT and protein levels in the urine. (See box 12.6 below). Only in patients with less than 1g of proteins. Used when CKD has not significantly progressed. --> increased risk can be kept under control. 
 

When blood of patient is pumped through set of semi-perm. membranes, bringing the blood into close contact with dialysate, where particles in excess flow out. Blood then flows back into patient. Dialysate can be adapted dependent on individual gradients per patient. 

Plasma water is removed, calcium, phosphate etc. And is replaced with solution of desired composition. Principle is still with semipermeable membrane. Employs counter-convenction, whereas dialysis employs convection. Removes larger particles like proteins that cannot be removed by haemodialysis. 

Dialysis that employs the peritoneal membrane as natural filter, where dialysate is pumped into peritoneal space and removes undesired serum products through differential concetration gradients. Is tolerated more by patients, cheaper, is less effective than haemodialysis but has high risk of infection. Therefore requires large patient complicance with hygiene measures.
 

Success of transplantation depends on:
- Blood compatibility (HLA)
- Immunosuppresive treatment
- Donor kidneys are ideally acquired from family.
- Cadaver transplants as well --> immunosuppresion.

Complications include:
- Tubular necrosis as most common cause of graft complications. 
- Technical failures.
- Acute rejection. 
- Infections
- Malignancy