Type 1 RTA pathophysiology, notes and mnemonic

Hello! This post is on type 1 renal tubular acidosis.

What causes Type 1 RTA?
Defective H+ ion secretion in the distal tubule.
Impairment in H+ ions secretion result in an inability to acidify the pH beyond 5.5 (Used in the diagnosis of type 1 RTA)


The plasma bicarbonate is significantly reduced and may fall below 10 meq/L.
These patients tend to have urinary K+ wasting and hypokalemia (thought to be due to increased potassium secretion by distal tubular cells in the setting of diminished H+ ion secretion.)

What type of RTA is associated with an enhanced chance if nephrolithiasis?
Distal or type 1 RTA can cause nephrocalcinosis / calcium oxalate kidney stones.
Mnemonic: ONE predisposes to stONEs

Pathophysiology: Hypercalciuria, hyperphosphatemia, nephrolithiasis (calcium phosphate stones) and nephrocalcinosis are frequently associated with untreated type 1 RTA. The hypercalciuria is thought to be due to:
1) increased calcium phosphate release from bone as a result of bone buffering of excess acid and
2) reduction in tubular calcium reabsorption secondary to chronic acidosis.
The hypercalciuria, alkaline urine, and reduced excretion of citrate in the urine (which normally prevents calcium crystallization) promote the precipitation of calcium phosphate and stone formation.

Which conditions are associated with type 1 RTA?
diStal RTA is associated with the 3 S's:
Sjogren's
SLE

Sickle cell anemia

Treatment: Bicarbonate administration

That's all!
-IkaN

How to remember Hepatitis B is associated with membranous glomerulonephritis

Writing this post because I confused it with focal segmental glomerulonephritis yesterday.

Hepatitis B is associated with membranous glomerulonephritis.

Mnemonic: Happy memory - Heppy membory - Hepatitis B Membranous nephropathy :D

That's all!
-IkaN

Aminoglycoside mnemonic

Hello all, let me slip in a quick mnemonic on Neomycin and Amikacin

1.Highest nephrotoxic drug-
   Neomycin

2.Highest auditory toxicity is with-
    Amikacin

N for N and A for A. Easy one to remember for the MCQs!

That's all!

-Sushrut

Principal cell: How to remember it's function and location in the nephron

Principal cell

Study group discussion: Skeletal resistance to PTH in CRF

Hi guys! So the question that was asked in the study group is- Why is there skeletal resistance to PTH in Chronic Kidney Disease?

Answer-

Skeletal Resistance to PTH has a multifaceted pathogenesis; the most imp factor being uraemia which screws with the PTH receptor's intracellular G-protein signaling mechanism in the Osteoblasts.

Dialysis in these patients increase the levels of Osteoprotegerin, which is a decoy molecule antagonizing the action of RANKL in promoting osteoclastogenesis; further intereference with the action of PTH.

Hyperphosphatemia and Hypocalcemia in CKD patients cause excessive release of PTH which leads to downregulation of its receptors on osteoblasts. 

Decreased levels of calcitriol screws in a special way, it makes the parathyroid gland think that the normal calcium level range is above the actual normal value, making the gland work overtime. For this we use calcimimetics like cinacalcet to decrease the set point back to the real normal value. And also without Calcitriol to assist, PTH's job becomes a lot more difficult. 

Earlier the most common CKD-related osteodystrophy was osteitis fibrosa cystica which was due to very high PTH levels causing pathologically increased bone turnover.

But now since we have developed drugs to tackle increased PTH levels, Adynamic Bone Disease has become the most common osteodystrophy because in the body of a CKD patient, it is already very difficult for PTH to carry out its function and if we are pharmacologically decreasing its values, we are ensuring that it works negligibly. 

That's enough Nephrology for one day! :)

  

-VM

Step 2 CK: Goodpastures syndrome notes

Hello!
Here's a short post on Goodpastures syndrome!

Contrast induced nephropathy notes

Features of contrast induced nephropathy

- Due to iodinated contrast agents (Other agents that cause AKI: Gadolinium for MRI, sodium phosphate solutions as purgatives)
- Prevented by use of non ionic contrast agents, IV hydration, acetyl cysteine.
- Serum Creatinine rises 24-48 hours after exposure. Resolves in a week.
- FeNa low, benign urinary sediment.
- Risk increases in CKD, Diabetic nephropathy, multiple myeloma.

Analgesic nephropathy notes

Analgesic nephropathy

Characterized by:
Renal insufficiency
Papillary necrosis

Due to:
Toxic drug levels in inner medulla
Causes chronic tubulointerstitial damage
Results from papillary ischemia due to vasoconstriction of medullary blood vessels (vasa recta)

Caused by:
Phenacetin containing preparations
Aspirin
Caffeine

Symptoms:
Polyuria (Due to impaired concentrating ability)
NAGMA (Due to tubular damage)
Hematuria (Due to sloughed necrotic papilla)
Sterile pyuria and WBC casts may also be seen
Ureteric colic, obstruction (Due to sloughed necrotic papilla)

At increased risk of:
Premature aging
Atherosclerotic vascular disease
Urinary tract cancer

That's all!
-IkaN

Alport syndrome notes

Alport syndrome notes

Membranous glomerulonephritis notes

Hey!
This post is on membranous glomerulonephritis :D

Erythropoietin therapy

Here are some important things you should know about erythropoietin therapy.

It is used in patients on dialysis.

Resistance to erythropoietin is most commonly due to iron deficiency.

Adverse effects are associated with rapid rise in hematocrit and hemoglobin - Hypertension, Thrombosis.

Other side effects are: Headache, flu like symptoms, red cell aplasia.

Did you know?

Erythropoietin was the first human hematopoietic growth factor to be isolated.

Erythropoietin was originally purified from urine of patients with severe anemia.

It is banned by the International Olympics Committee.

That's all!
-IkaN

Nephrotoxic antimicrobials

Hello! In this post, I'll be talking about nephrotoxic antimicrobials.

Let's start with Aminoglycosides!

Aminoglycoside toxicity manifests in the form of tubular necrosis.

Did you know AKI due to Aminoglycosides manifest 5-7 days after therapy even after the drug has been discontinued? :O

Aminoglycosides accumulate in the renal cortex and cause non oliguric AKI. Hypomagnesemia is a common finding.

Amphotericin B also causes tubular necrosis. It binds to tubular membrane cholesterol and introduces pores. Clinical findings include polyuria, hypomagnesemia, hypocalcemia and NAGMA.

Mnemonic for nephrotoxic drugs: Drugs with A!

Aminoglycosides
Amphotericin B 
Antivirals like acyclovir, tenofovir, cidofovir, foscarnet, pentamidine.
(Cause tubular toxicity)

Antibiotics like penicillin, cephalosporins, quinolones, sulfonamides, rifampin.
(Cause acute interstitial nephritis)

Remember, in acute interstitial nephritis, WBCs, WBC casts and urine eosinophils will be seen. However, in AKI, the urine sediment will show granular casts.

That's all!
The predominant feeling I have is that if gratitude (=
-IkaN

Radiolucent stones mnemonic and uric acid calculi

Good morning! =)

I was studying about radiolucent kidney stones and thought of sharing what I learnt with you all.

Mnemonic for radiolucent renal calculi: CATIX URL
Cysteine
Adenine (2,8-Dihydroxyadenine)
Triamterene
Indinavir
Uric acid
RadioLucent

Another mnemonic for medication stones: GUEST MIC
Guaifenesin stones (Radiolucent)
Ephedrine stones (Radiolucent)
Sulphonamides stones (Radiolucent)
Triamterene stones (Poorly radiopaque)
Magnesium trisilicate stones (Poorly radiopaque)
Indinavir stones (Radiolucent)
Cephalosporins stones (Radiolucent)

If you are asked to choose the radiolucent one between Orotic acid stones and cysteine stones, choose orotic acid. It is radiolucent, cystine is poorly radioopaque.

Magnesium ammonia phosphate (struvite) and Cystine calculi are less radiodense and are more difficult to visualize. Uric acid, orotic acid, xanthine, triamterene, dihydroxy­adenine, and indinavir calculi are radiolucent and might not be seen on a plain radiograph.
(Source.)

Predisposing factors for uric acid stones:
1. Low urinary pH
2. High uric acid excretion

Treatment for uric acid stones:
1. Alkalinization of urine
(Sodium bicarbonate, potassium citrate)
2. Increase fruits, veggies. Decrease animal flesh.
3. XOI - Allopurinol, Febuxostat

Alkalinization of urine mnemonic: ABC.
Alkalinization. Bicarbonate. Citrate.
(Sodium bicarbonate and potassium citrate are used for alkalinization of urine)

That's all!
-IkaN

SAAG mnemonic

Hello!

SAAG is serum albumin ascites gradient.

SAAG is >1.1 in portal HTN, CHF, HVT and constrictive pericarditis.

The mnemonic for this is SAAG is High in conditions with an H.

portal Hypertension
congestive Heart failure
Hepatic vein thrombosis
Heart constriction (Constrictive pericarditis)

For completion, SAAG < 1.1 is seen in nephrotic syndrome, cancer and infections (except SBP)

That's all!
Have an amazing day!
-IkaN

Study group discussion: ACEI and bilateral renal artery stenosis

Angiotensin converting enzyme inhibitors (ACEI) are contraindicated in bilateral renal artery stenosis. Why?

In renal artery stenosis, renal perfusion is less and hence GFR is low. In such a case, nephrons adapt the filtration by causing efferent arteriolar constriction to maintain the pressure needed for filtration.
If ACEI is given, there is dilation of efferent arteriole and renal perfusion will again decrease further and GFR will become more low. Hence, contraindicated.

In bilateral renal stenosis, the effective renal blood flow is not significantly reduced but maintained at the cost of increasing the efferent artery tone. ACEI causes inhibition of angiotensin 2, leading to efferent artery vasodilation in glomerulus. This decreases intra glomerular pressure and filtration, resulting in renal  function detoriation.

Hodgkins lymphoma and minimal change disease mnemonic

Which nephrotic syndrome is associated with Hodgkins lymphoma?

Lymphoma usually causes membranous nephropathy.

But Hodgkins is a weirdo which minimal change disease.

Mnemonic: Kids get MCD usually, so "Hodgkid"

Mnemonic by DJ AweSpear sent to us in our study group. Thanks!

Membranous glomerulonephritis mnemonic

Most common cause of nephrotic syndrome in adults.

Associated with clots - DVT, renal vein thrombosis and PE are common.

Nephrotic syndrome associated with malignancy.

It's membranous glomerulonephritis! :D

Approach to acid base disorders: Metabolic alkalosis notes

In suspected metabolic alkalosis, always check urinary chloride levels.

Metabolic alkalosis associated with a reduction in the ECV (Vomiting, diuretics):
There will be a stimulus for Na and Cl reabsorption to replenish extracellular volume.
Urinary Cl is very low ( < 25 meq/L).
Administration of NaCl and water leads to correction of the metabolic alkalosis.
Such causes of metabolic alkalosis are said to be saline responsive.

Approach to acid base disorders: Metabolic acidosis notes

Hello!

I made these notes while studying acid base disturbances. Now they might not make sense to someone who has never studied this topic before.. But for those who have read about it, this should be excellent for revision.

Calculation of anion gap:
ALWAYS calculate the anion gap first.
Anion gap = [Na+]  − ([Cl-] + [HCO3−])
Normal anion gap = 8 - 16 mEq / L

What causes renal bruit?

Narrowing of the renal artery (Renal artery stenosis) causes renal bruit.