Haematology and kidney disease

The kidney maintains:
 volume of plasma
 concentrations of
electrolytes
 pH within physiological
range
 Achieved by varying amounts
of water and salts excreted.
 Excretes waste products (e.g.
urea, creatinine and
urobilinogen)
What proportion of the body's ATP does it use for all of these functions?

What is the lifespan of an erythrocyte?

Which organs/tissues are included in the reticuloendothelial system (extravascular system in which macrophages phagocytose erythrocytes and recycle iron)?

Briefly describe the breakdown of haem from erythrocytes.

Intravascular haemolysis plays little role in normal erythrocyte destruction as erythrocyte metabolism and iron recycling occurs in the extravascular reticuloendothelial system. Which diseases is intravascular haemolysis associated with?

Macrophages are not really involved in intravascular haemolysis. Which blood components bind to erythrocytes and result in their lysis?

Haemolytic anaemias are characterised by an increased rate of erythrocyte destruction. What clinical feature might result if there is too much erythrocyte destruction (not anaemia...)?

What is methaemalbumin?

What is haemosiderinuria?

In haemolytic anaemias, is erythrocyte destruction intravascular or extravascular?

How might anaemias be 'masked'?

Defects in erythrocytes which result in their premature destruction are usually inherited. List three conditions in which erythrocytes are defective and which may result in haemolytic anaemias.

Why do erythrocytes only have the haemoglobin/enzymes that they start their lifespan with?

List some acquired causes of haemolytic anaemias.

Haemolytic transfusion reactions are reactions to 'foreign' blood with previously 'unseen' antigens in which there is increased haemolysis. This breakdown may be intravascular or extravascular - what does this depend on?

What are the signs of a haemolytic tranfusion reaction? What is the timescale?

In fatal cases of haemolytic transfusion reactions, death may result from disseminated intravascular coagulation (DIC) and associated hypotension, or from acute renal failure. What is the basic pathogenesis of DIC?

Which hormone does the kidney produce to regulate erythropoiesis?

What about the bone marrow might affect erythropoiesis, resulting in anaemia?

Which nutrients are critical for erythrocyte formation?

How can respiratory dysfunction result in anaemia even if Hb concentration is fine?

Erythropoietin production increases in anaemia. Describe some other situations in which it will increase.

Renal failure can affect EPO production, resulting in impaired erythrocyte production and a normochromic anaemia. What factor in the serum may result in the formation of 'spur' and 'burr' cells? Why?

What is a Burr cell technically called? And a spur cell?

Here are some erythrocyte structural abnormalities and their causes.

There are other factors affecting the anaemia caused by dialysis in chronic renal failure. What do these include?

What is the basic process by which thrombopoiesis is increased?

As well as producing erythropoietin and a small proportion of thrombopoietin, what other hormone do they kidneys produce?

Renin controls blood pressure through the renin-angiotensin system. How?

So kidney disease can cause haem problems (e.g. reduced EPO production) but haem can cause kidney problems too - namely disturbances in cell differentiation in the bone marrow, such as multiple myeloma. How does this result in kidney disease?

Multiple myeloma (MM) is a neoplastic proliferation of plasma cells in the bone marrow, resulting in their accumulation as well as presence of monoclonal protein (antibody
molecules and/or free light chains) in serum and urine as malignant plasma cells have clonally re-arranged Ig genes and secrete excess paraprotein. Why are IL-6 and osteoclast activating factor (OAF) significant in multiple myeloma?

What do multiple myeloma plasma cells and the Philosopher's stone have in common?

List some of the clinical features of multiple myeloma.

Why is there an increased infection risk in multiple myeloma?