.RU

So, fever, flank pain, and WBC casts = ACUTE PYELONEPHRITIS - Chapter 1: Cellular reaction to Injury


So, fever, flank pain, and WBC casts = ACUTE PYELONEPHRITIS.

So, its an

ascending infection due to incompetent vesicouretal junc

. This usually shows up in newborn girls (and will be a prob for rest of lives).

Example: kidney with white spots = abscesses seen in pyelonephritis. If you have constant acute attacks of pyelonephritis, can become chronic. Therefore have increased risk of HTN and renal failure.

B. Chronic Pyelonephritis



Example: scarred kidney (on cortex), blunting of the calyces (occurs under the scar), seen on intravenous pyelograms – dx? CHRONIC pyelonephritis. So,

blunting of the calyces = CHRONIC pyelonephritis.



C. Acute Drug-induced interstitial nephritis



Can

drugs

produce a nephritis involving the interstitium and tubules? Yes – can be acute and chronic and ez to diagnose. Why? B/c will have

fever, and develop a rash.

Fever + Rash

(obviously due to drug, b/c started after taking the drug),

oliguria

,

eosinophiliuria

(

eosinophils in the urine – pathognomonic

). This is called

acute drug induced interstitial nephritis

. This is more and more common, and is a very common cause of chronic renal failure. So, put pt on drug, get fever, rash, oliguria = discard/stop drug (never give again) – this is a combo of type I and IV HPY.

Analgesic nephropathy



Example: discoloration in renal medulla, pale infarct, renal papilla sloughed off – ringed signed; and on pyelograms there will be nothing there just an empty space. Dx?

Analgesic nephropathy

. This

from combo of acetaminophen and aspirin over a long period of time.

Acetaminophen

is producing free radicals. B/c of the poor circulation in the medulla, there is free radical damage on the tubular cells of the medulla.

Aspirin

will block PGE2 (a vasodilator), therefore angiotensin II (a vasoconstrictor) is in charge of the renal blood flow. Vasoconstrictor of the efferent arteriole. The peritubular capillaries arise from the efferent arteriole. So, with vasoconstriction of the efferent arteriole, pt is affecting peritubular capillaries going around collecting tubules and renal medulla. So, is that producing ischemia? Yes. So, pt

has free radical damage and ischemia leading to analgesic nephropathy

. This is why the renal papilla necroses, sloughs off, and leads to

renal

papillary

necrosis

. So,

aspirin and acetaminophen toxicity. Diabetic nephropathy (b/c causes ischemia), acute pyelonephritis (b/c abscess formation), SCDz and trait, can all lead to analgesic nephropathy.



XV. Chronic renal Failure



Definition

: Pt has BUN/Cr ratio 10:1 for more than 3 months

. If both kidneys failed: will not be able to excrete the things we normally get rid of (so those

things will build up

– ie salt); EPO production will decrease, leading to

normocytic anemia with a corrected reticulocyte ct of less than 2%

. Will not be able to get rid of organic acids, leading to

metabolic acidosis

, increased anion gap. With metabolic acidosis, bones try to buffer all the acid. B/c the bones are buffering the extra H ion, bone dz can develop, leading to

osteoporosis

. The prox tubules are messed up in the renal tubules, and 1-alpha hydroxylase will decrease (this responsible is hydroxylating Vit D); so, with renal failure will also have

hypovitaminosis D

(vit D def). This means that there will be

hypocalcemia

and

hypophosphatemia

, leading to

osteomalacia

. So, there are two bone dz’s – osteoporosis (b/c buffering and wearing away bone matrix) and osteomalacia; also, PTH is reacting to chronic hypocalcemia and leads to

secondary hyperparathyroidism

(also affects the bone). The bun/Cr ratio is 80/8. So, if you know normal renal func you know what happens.

XVI. Other Problems related to kidneys:



Example: pt has essential HTN over 10 yrs, and pt is not compliant with medication – kidney with cobblestone appearance =

nephrosclerosis

. Underlying dz causing it: hyaline arteriolosclerosis b/c there is decreased blood flow, tubular atrophy, glomeruli are fibrosing off, renal function is going down, and leads to renal failure.

Example: lets say the pt wakes up with a big headache and blurry vision. Pt is getting dizzy, goes to dr, and pressure is 240/140, in the retina, dude has papilloedema with flame hemorrhages and hard and soft exudates, grade 4 hypertensive retinopathy, BUN/Cr are 80/8 –

dx? Malignant HTN

(aka flea bitten kidney – petechia visible on surface of kidney – see vessel changes ie hyperplastic arteriolosclerosis, and the BV’s are rupturing, leading to petechial lesions on the cortex – called flea bitten kidney). This is all you have to know. They can also ask

Rx: IV nitroprusside to get the BP down

. So, they have CNS edema with papilloedema, and if the BP isn’t lowered, they are gonna die.

Example: kidney with abnormal areas that are pale and depressed – so, if you take a section through one of these, and you see an irregular irregular pulse, will see pale infarction with coagulation necrosis b/c what you are looking at are

infarcts

. Irregular irregular pulse is from atrial fib, and atrial fib is most dangerous for

embolization

. So, these infarcts are from

multiple emboli

, leading to multiple

pale infarcts of the kidney. This is NOT pyelonephritis b/c has microabcesses

Example: atrophy due to dilatation of the renal pelvis, leading to

hydronephrosis

.

So, if you have hydronephrosis and increased pressure pressing on the cortex and medulla, what happens to that?

Get ischemia and atrophy – which is called compression atrophy.

This is very similar to cystic fibrosis ducts filled with mucous – the pressure is impacted back to the glands, and they undergo compression atrophy. Cortex and medulla are very thin, along with very dilated renal pelvices.

MCC = stone



Example:

staghorn calculus – urine pH is alkaline and smells like ammonia; therefore, there must be a urease producer, and this is Proteus. B/c it is a urease producer,

they break urea down to ammonia, and get an alkaline pH. This is why a

staghorn calculus is Mg ammonium phosphate

, and only develops in infections in pts that have urease producers. E coli are not urease producer and proteus species are and they predispose to these stones. Do not pass these stones (too big), therefore need to extract these (surgery). So,

urease producer, alkaline pH, ammonia smell to the urine.



XVII. Tumors of the kidney



If you see a mass in a kidney, and its an adult, it is a

renal

adenocarcinoma

. If it’s a kid, it’s a wilm’s tumor. So, if you see a mass in the kidney, its prob not mets (b/c not many things go there), its not b9, pick cancer.

So, adult = renal adenocarcinoma, kid =

w

ilms tumor; they derived from the proximal tubule and the MCC = smoking; they make lot of ectopic hormones: EPO, parathyroid hormone (leads to hypercalcemia), invade the renal vein.



Cells are clear, full of glycogen.



Example: flank mass in child, HTN = Wilms tumor; HTN occurs b/c it’s making renin; usually unilateral. Histology: cancer where pt is duplicating embryogenesis of a kidney – everything is primitive. Can see rhabdomyblasts; likes to mets to lung

If

AD, from c’some 11, and have 2 classic findings: aniridia (absent iris), and hemihypertrophy of an extremity (one extremity is bigger than another) – this is a sign that the wilms tumor has a genetic basis.



Papillary lesion in the bladder = transitional cell carcinoma (TCC)

What is the MCC transitional cell carcinoma of the bladder? Smoking

Dye use to look? Aniline dye; what is chemotherapy agent used to Rx Wegener’s? Cyclophosphamide. What are the complications of Cyclophosphamide? Hemorrhagic cystitis and transitional cell carcinoma.

How do you prevent this? Mesna.

XVIII. Urinary Tract Infection



MC urine abnormality seen in the lab

Example: arrow pointing to neutrophils in urine; RBC’s in it, too, bacteria – E coli (play odds). So,

see neutrophils, RBC’s and bacteria. The dipstick will pick up all three of these things.



+” dipstick for blood due to RBCs

. Hematuria is very frequent and sometimes a lot of blood comes out (

hemorrhagic

cystitis

) and most of the time its

E coli

, but sometimes it can be from adenovirus.

Also, the

dipstick has leukocyte esterase

and it’s measuring the enzyme in the leukocyte.

Most urinary pathogens are nitrate reducers, meaning that they convert nitrate to nitrite. On a

dipstick, they have a section for nitrites

. B/c E coli is a nitrate reducer, there should be nitrites in the urine, which are dipstick “+” for that.

So, you have a pt, woman or man, who has dysuria, increased frequency, suprapubic pain and have a urine sediment of neutrophils, RBC’s, bacteria or dipstick findings of hematuria, leukocyte esterase pos, nitrate “+”

= UTI



Is it lower or upper? If the pt has fever, flank pain, WBC casts its upper, if none of these things are present, its lower.



Example

:

pt with dysuria, increased frequency, neutrophils in the urine, few RBC’s, no bacteria, “+” leukocyte esterase, urine culture is neg, and sexually active person, dx?

Chlamydia – normal urine cultures do not pick up Chlamydia trachomatis. It is the MC STD.

In men, called nonspecific urethritis, in woman its called acute urethral syndrome. We also use the term called sterile pyuria. We don’t have bacteria present, but do have neutrophil present. On routine stool culture, its neg. So,

one cause of sterile pyuria is Chlamydia infection and the other one is TB.



MC organ that military TB goes to = kidney, therefore will have TB in the urine, and it will be sterile b/c urine cultures do not pick up. So, remember Chlamydia and TB as causes of sterile pyuria.

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