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HMS Homeostasis II > Diabetes IV - Renal Manifestations > Flashcards

Diabetes IV - Renal Manifestations Flashcards

1
Q

Common causes of nephrotic syndrome

A
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2
Q

Anti-GBM disease summary

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3
Q

Membranous nephropathy summary

A
  • Nephrotic syndrome
  • Caused by sub-epithelial IC formation within the urinary space and subsequent basement membrane proliferation
  • Most common in adults
  • EM: “Spiked” pattern of BM with large, sub-epithelial, electron dense deposits
  • IF: Granular staining with IgG and C3 (usually IgG4)
  • Can be primary or secondary
    • Primary is idiopathic
    • Secondary: caused by autoantibodies that were generated in response to infection, malignancy, autoimmunity, or medications
  • Treated by addressing underlying cause if secondary, or with steroids if primary
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4
Q

IgA nephropathy summary

A
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5
Q

Hydroureter and hydronephrosis

A

Hydroureter: dilation of the ureter due to distension with fluid

Hydronephrosis: dilation of the renal pelvix and misshapen papillae due to distension with fluid

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6
Q

Primary vs secondary FSGS

A
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7
Q

Common causes of nephritic syndrome

A
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8
Q

Clues that you are dealing with idiopathic or adaptive FSGS

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9
Q

Membranous glomerulonephritis summary

A
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10
Q

The dynamics of K+ in the pathophysiology and management of DKA

A
  • At the onset of symptoms, insulin deficiency causes a shift of potassium out of cells
  • However, potassium is also lost due to diuresis with glucose and ketones
  • These urinary losses are then limited due to RAAS activation after a period of water loss, resulting in reduced distal Na+ delivery
  • Treatment: Potassium is likely to fall with the infusion of saline to treat volume depletion, as RAAS activation will diminish and distal Na+ delivery will increase. Insulin administration will also cause K+ to fall as it is shifted intracellularly.
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11
Q

If a diabetic patients presents with HHS, what affect will treating the HHS have on serum sodium?

A

Sodium will go up.

Doesn’t matter if they are hyponatremic, normonatremic, or hypernatremic.

As glucose re-enters cells, it will take water with it, decreasing the volume in which the extracellular sodium is dissolved.

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12
Q

Risks of using RAAS blockers in slowing progression of diabetic nephropathy

A

In the short term, GFR will be worse! Creatinine will rise due to interference with GFR-preserving RAAS mechanisms. However, this will soon be compensated for and proteinuria and blood pressure will decrease.

There is also an increased risk of AKI given that we are blocking a protective mechanism for low-flow conditions, as well as hyperkalemia since we are blocking the principal mechanism of aldosterone production.

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13
Q

In diabetes, the initial insult to the kidney is . . .

A

. . . local damage to the glomerular capillaries, characterized by thickening of GBM. This will present as “hyperfiltration,” and reduced creatinine, but accompanied by microalbuminuria.

Ultimately, this will progress to podocyte stretching, apoptosis, and secondary focal and segmental glomerulosclerosis with declining renal function.

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14
Q

Acute post-infectious glomerulonephritis summary

A
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15
Q

Expected renal compensation for a respiratory acidosis

A

Acute: [HCO32-] = (pCO2 - 40)/10 +24

Chronic: [HCO32-] = (pCO2 - 40)/3.5 +24

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16
Q

Correcting serum sodium for hyperglycemia

A

Measured sodium [mEq/L] + 0.016 * (Serum glucose [mg/dL] - 100)

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17
Q

ANCA-associated glomerulonephritis summary

A
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18
Q

Conditions that cause secondary focal and segmental glomerulosclerosis

A
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19
Q

Primary focal and segmental glomerulosclerosis summary

A
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20
Q

Delta/Delta

A

The change (or increase) in the anion gap compared to the change (or fall) in the bicarbonate. This is a tool to determine if there is yet another underlying disorder.

21
Q

Why is it so important to differentiate primary and secondary FSGS?

A

Treatments! The treatments are so different.

For primary, immunosuppression is indicated.

For secondary, RAAS blockade is indicated.

22
Q

Diabetic nephropathy summary

A
23
Q

Extraglomerular aspects of diabetic nephropathy

A

Vascular disease as well due to thickening of the vascular media and sclerosis of the tubulointerstitium

Nodules and glomerular walls will also stain lightly with IgG, as well as albumin. This is just due to the “stickiness” of the glycosylated matrix.

24
Q

Amyloid nephropathy summary

A
25
Q

Other (non-diabetes) etiologies of KW nodular glomerulosclerosis

A

Heavy smoking

26
Q

In order for the kidney to compensate for glomerular loss, what must be changed to preserve GFR?

A

Ultimately, the average SNGFR will need to go up. But, the only way to do this in the short-term (given all of the physical limitations of the kidney) is to increase ΔP in the glomerular capillary space.

This increase in glomerular pressure then results in glomerular hypertrophy, increasing the SA available within each glomerulus.

27
Q

How does extensive glomerular hypertrophy gradually lead to proteinuria?

A

If the glomerulus becomes too hypertrophied and pressure remains high, then podocytes may be squished aside or too thinly stretched, widening filtration slit diaphragms and allowing protein to escape into the urine. This then may result in podocyte apoptosis and segmental scarring.

This then results secondary focal and segmental glomerulosclerosis, accompanied by tubular atrophy and interstitial fibrosis. However, these patients tend not to present with the nephrotic syndrome.

28
Q

The soluble factor that causes minimal change disease and possibly also primary focal and segmental glomerulosclerosis is believed to be made by ___.

A

The soluble factor that causes minimal change disease and possibly also primary focal and segmental glomerulosclerosis is believed to be made by T cells.

This is why immunosuppression is effective in treatment of these diseases.

29
Q

Renal toolbox

A
  • Serum anion gap (Na - [Cl + HCO3])
  • Urine anion gap (Osm - 2[Na+K])
  • Delta/delta (ΔAG / ΔHCO3)
30
Q

Hypernatremia may develop in some patients with HHS, and in these cases it is usually due to ___.

A

Hypernatremia may develop in some patients with HHS, and in these cases it is usually due to osmotic diuresis without replenishment.

31
Q

Assessing volume status in infants

A

Body weight and the fontanelle!

In severe losses, the skin can be mottled or cool to touch and the fontanelle may be “sunken”. The urine output may decrease

32
Q

Diabetic patients in HHS are likely to have ___ sodium.

A

Trick question!

There is no relationship between HHS and sodium. HHS patients may present with any level of sodium depending on the severity of the HHS and how much water the individual consumed.

33
Q

Lupus nephritis summary

A
34
Q

HARDUP pneumonic for non-anion gap acidoses

A
  • Hyperalimentation - too acidic parenteral nutrition
  • Acetazloamide
  • Renal (I, II, IV, or CKD)
  • Diarrhea
  • Ureterosigmoid fistula
  • Pancreatic fistula
35
Q

Major nephron pathologies broken down by syndrome

A
36
Q

What changes are there in GFR, proteinuria, and serum creatinine after placing a type II diabetes patient with microalbuminuria from early diabetic nephropathy on an ACE inhibitor?

A

GFR will decrease slightly, but creatinine will decrease and proteinuria will decrease or disappear.

ACE inhibitors will prevent or at least limit further remodeling.

37
Q

In diabetic nephropathy, what would you see on a glomerular ultrastructure?

A

Depends where you look!

You should see pretty regular membrane expansion, but depending on where you biopsy you may or may not see podocyte foot process disarray.

Meanwhile, if you had a patient with primary focal and segmental glomerulosclerosis, food process pathology would be diffuse, even in apparently unaffected glomeruli.

38
Q

Using the delta/delta

A

DD Ratio <1.0 = presence of concurrent non AG metabolic acidosis.

DD Ratio >2.0 = presence of concurrent metabolic alkalosis.

39
Q

Membranoproliferative glomerulonephritis summary

A
40
Q

Expected respiratory compensation for metabolic acidosis and alkalosis

A

Acidosis: pCO2 expected = 1.5 x [HCO32-] + 8 +/- 2

Alkalosis: pCO2 expected = 0.7 x [HCO32-] + 21 +/- 1.5

41
Q

Vesicourethral reflux

A

When the one-way valve of the ureterovesicular junction fails, usually due to an anatomical abnormality, and results in urine propulsion up the ureter to the kidney.

If there is a limited cystitis, this may result in progression to a pyelonephritis, or in other words a polar infection of the kidney (polar because of the high susceptibility of the polar compound papillae of the kidney). This may result in polar scaring and kidney shrinking and eventually kidney failure.

42
Q

Mechanism of hyperosmolar hyponatremia

A

Normonatremia, then add glucose to the blood

Water follows

Salt is diluted

Ergo, hyperosmolar hyponatremia

43
Q

Minimal change disease summary

A
44
Q
A
45
Q

Where does ketone synthesis occur during DKA and what is a targetable enzyme in this pathway?

A

Ketone synthesis occurs in the mitochondria of the liver, with HMG-CoA Synthase being a targetable enzyme in this pathway.

46
Q

How can diabetic nephropathy be prevented or delayed?

A
  • ACE inhibitors
  • ARBs
47
Q

What is going on in this kidney biopsy?

A

Diabetic kidney disease

The mesangial nodules seen are called Kimmelstiel-Wilson nodules, and are the result of early diabetic neuropathy’s basement membrane proliferation.

Don’t be fooled! It may look similar to IgA nephropathy, but look closer and see that there are true nodules of acellular basement membane, where in IgA the mesangial cells proliferate as well.

48
Q

Normal # of nuclei per mesangial lobule

A

~2-3

49
Q

Main treatment of any form of secondary FSGS

A

RAAS blockade

HMS Homeostasis II (35 decks)

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