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2023 S2 Renal Practical CSB520

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Renal Practical

Hereditary: Transmitted via gametes (sperm/ova), therefore familial.


Congenital: Present at birth.
Not all genetic disorders are congenital (appear at birth) & not all congenital disorders are genetic.

Evolution and inheritance: Genetic mutations can propagate within a population only if they do not interfere
with our ability to replicate, for example if I have a novel mutation, it disappears with me if I do not pass it on
to the next generation. In the case of many disorders, genetic screening can ensure the birth of a child that is
neither affected with or a carrier of the disorder and yet many conditions prevail.

Autosomal recessive inheritance: Diseases that show autosomal recessive inheritance will continue even if
they impair fertility. This is due to the fact that to have these diseases you must inherit 2 mutated alleles, one
from each parent, if you only have one then you are an asymptomatic carrier of the condition.

Autosomal dominate inheritance: The ability of diseases with autosomal dominant inheritance to prevail
within a population is dependent upon their ability to interfere with fertility, however, many autosomal
dominant diseases only exhibit clinical symptoms in the 3rd to 5th decade of life, after a person has
propagated and thus potentially passed on the gene.

1.0 Horseshoe kidney


An incidental autopsy finding - no clinical problem resulted.

1.1 Adult Polycystic kidney disease


The kidney is normal during childhood and early adult life but then cysts develop and typically cause chronic renal failure beginning
at age 40 - 60 years.
Question 1

a. What has happened to the normal renal parenchyma in response to the formation and growth of the
cysts?
B. Neoplasms
2.0 Nephroblastoma (Wilms’ tumor)
Nephroblastoma excised surgically from a boy aged 5 and half years of age. This type of malignant tumour occurs in children, usually
before their fifth year of life. Hypertension, pain and haematuria are common symptoms associated with this tumour.

2.1 Primary renal cell carcinomas


2.2 Papillary carcinoma of the ureter with kidney showing hydronephrosis & cysts
2.3 Papillary Bladder carcinoma
Benign hyperplasia of the lateral and middle lobes of prostate has caused hypertrophy of the bladder wall, which shows
trabeculation and diverticula.

Question 2

a. What does the term ‘blast’ denote?

b. The cancers in 2.2 and 2.3 are named papillary as they are growing in a papillary structure, what would
be the appropriate name based on their cell of origin?

c. Why are the names of the cancers in 2.0, 2.1 and 2.2 not the same?

d. Why are cancers of the kidney, ureter and bladder generally diagnosed late, what signs and symptoms
do patients present with?

C. Tubular-Interstitial & Glomerular Diseases


3.0 Pyelonephritis
Extensive acute suppurative (pus present) pyelonephritis and papillary necrosis.

3.1 Chronic pyelonephritis


Chronic pyelonephritis with a still adherent necrotic papilla in the lower calyx. Chronic pyelonephritis follows acute in many cases.
The kidney in chronic pyelonephritis may look like the kidney in chronic glomerulonephritis, in both cases renal failure is the likely
outcome if both kidneys are affected.
Question 3

a. Routes of entry for microbes infecting the kidney include haematogenous (descending) and urinary
(ascending) spread, what are the most significant differences between these?

b. Why is pyelonephritis more common in females than in males?

c. What is the papilla and why does it become necrotic?

3.2 Glomerulonephritis – acute


Acute glomerulonephritis often leads to the chronic condition and renal failure.

3.3 Chronic glomerulonephritis


Granular (rough surface) contracted (small because of ischaemic atrophy and scarring) due to chronic glomerulonephritis, which
follows as a consequence of acute glomerulonephritis.

3.4 Chronic glomerulonephritis (end stage kidney) (H&E) Note the massive reduction in both the number and size of
tubules (tubular atrophy) and progressive hyalinisation and loss of glomeruli. Hyaline is a complex of trapped plasma proteins,
increased mesangial matrix, basement membrane material and collagen.

d. Why does glomerulonephritis typically affect both kidneys?

e. Why does glomerulonephritis often lead to chronic renal failure?


f. Describe the impact that renal failure has on the rest of the body, pay particular attention to the
effects on the haematological, cardiovascular and skeletal systems:
D. RenalCardiovascular Disease
4.0 Nephrosclerosis
Senile contracted kidneys. Diffuse small ischaemic infarcts within the kidney result in scarring. This commonly accompanies
hypertension and may be exacerbated by the renal arterioles becoming very muscular (sclerosis) and reducing renal perfusion
leading to further ischaemic atrophy and necrosis.

4.1 Renal infarction


Recent renal infarct in a woman aged 56. Note the thrombosed artery. Normal kidney tissue surrounding the infarcted area
responds with acute inflammation as part of the defence-repair process.
Question 4

a. What are the risk factors for atherosclerosis that are prioritized in the cardiovascular risk charts?

b. How do the kidneys respond to hypotension?

c. Explain the relationship between systemic hypertension and renal damage.


E. Urolithiasis (Calculi or Stones)
5.0 Staghorn renal calculus.
Staghorn calculus: the 'stag horn' shape is determined by the pelvis in which the calcium salts are precipitating. Once a stone
(urolith) forms, this becomes a focus or nidus on which further precipitation occurs.

5.1 Urolithiasis
Impacted stone (urolith) in the ureter - note the chronic inflammatory response leading to thickened ureteric walls. Contraction of
the chronic proliferative inflammatory tissue (scar) in the wall of the ureter has produced a ureteral stricture. Hydronephrosis: back
pressure of urine has caused extensive loss of renal tissue, enlargement of the renal outline and accumulation of fluid in the dilated
spaces.

5.2 Bladder calculus


Obstruction of the bladder outlet results in some urine being retained after micturition.

5.3 Hydronephrosis
Kinking of the pelvic-ureteric junction has produced a unilateral obstruction and hydronephrosis.

Question 5

a. Would the condition described in 5.3 have led to renal failure?

b. What are the main causes of urinary stone formation?

c. What are the potential causes of urinary stone formation?

d. Apart from stones, what else could cause hydronephrosis?

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