Minimal Change Nephropathy

Minimal Change Nephropathy (MCN)

There are a few common questions for MRCP Part 1 and 2 about nephrology, minimal change nephropathy is one of them.

There are a few important facts to remember,

1) Minimal change nephropathy is the commonest cause of nephrotic syndrome in children as well as in adult. Another important cause of nephrotic syndrome in adult is Focal Segmental glomerulosclerosis.

2) Minimal change literally means the kidney biopsy of  MCN will be normal unless your have electron miscroscope which shows efficement of foot processes.

3) More than 90% will respond to steroid.

4) There are a few secondary causes of minimal change nepropathy causing nephrotic syndrome- Gold, penicillamine, tumour etc

If a patient with nephrotic syndrome patient comes in with severe abdominal pain, always think of

1) Renal vein thrombosis
2) Spontaneous bacterial peritonitis

Hemoglobinuria or myoglobinuria

Hemoglobinuria and myoglobinuria

I always confused these two conditions when I was a medical student. Now let me make these conditions as simple as possible.

Hemoglobinuria just means presence of hem in the urine whereas myoglobinuria means presence of myoglobin in the urine. Both can cause acute kidney injury due to pigment nephropathy.

Remember that both can cause a false positive in urine dipstick for RBC. Patients with both these conditions produce tea coloured urine. However myoglobinuria may be differentiated from hemoglobinuria by performing a series of simple tests.

-Myoglobinuria is brown, and often only a few RBCs are present in the urine.
-Hematuria produces a reddish sediment in spun urine samples.
-Red or brown urine with a negative dipstick result for blood indicates a dye in the urine.
-Hemoglobin produces a reddish or brown coloration in the spun serum, whereas myoglobin does not discolor the serum.
-CK levels are markedly elevated in myoglobinuria.

Another common question in MRCP- if you notice red to brown urine with negative dipstick, there are only a few possibilities- bladder analgesic phenazopyridine or a variety of other medications, certain food dyes, the ingestion of beets in susceptible subjects, porphyria and hydroxocobalamin for the treatment of cyanide intoxication.

Question in MRCP

A 17 year old male with glucose-6-phosphate dehydrogenase deficiency presents with tiredness and is noticed to
be jaundiced. These features have developed since he developed a mild chest infection one week ago. Which one
of the following is the most likely haematological finding?

1 ) Haemoglobinuria
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film

Answer: 1

Tumour Lysis Syndrome in MRCP

Tumour Lysis Syndrome in MRCP

OK, this is a popular problem you see during your internship if you are working in an oncology ward. Remember that it is a MEDICAL EMERGENCY!

Tumor lysis syndrome (TLS) describes a condition with significant clinical and lab abnormalities caused by rapid and massive tumor cell death. Occurring either spontaneously or after chemotherapy. Therefore, it is quite logical to get this in patients with very high tumour load ( such as leukemia or lyphoma with very high white cell load)

You always encounter this syndrome post chemotherapy and always suspect this if patient develops acute kidney injury and hyperkalemia post chemotherapy.

Due to massive cell lysis, you will anticipate patients to have hyperkalemia, high phosphate and high uric acid with low Calcium.

Sometimes, patients might just present with seizure or cardiac arrthymias.

The pathogenesis of acute kidney injury is not so important for MRCP Part 1 and 2. Anyway you might get some ideas from the photo below,

About the amanegement, it is easy, the principles are below,

1) Adequately hydrate patient to prevent cystals formation

2) Prevent/minimize uric acid formation by giving allupurinol or rasburicase.

and of course sometime, you might need to dialyse the patient.

Bartter's and Gitelman's Syndromes

Bartter's and Gitelman's Syndromes in MRCP

I hate syndromes because I always can't remember them well. My Professor once said, clinicians term something as syndrome when they do not know much about an illness.

Having said that, some syndromes are important for your MRCP,I am going to talk about Bartter's and Gitelman's syndrome.

First fact to remember, Bartter's syndrome is an disorder of transport in the medullary thick ascending limb of Henle.

Second fact to remember, Bartter's syndrome is an illness resembles patients chronically takingloop diuretcs that inhibit activity of Na-K-2Cl co transporter.

Third fact to remember- they do not have hypertension.

So, what will happen to you if you chronically take frusemide?

Easy- you get hypokalemia and alkalosis and hypercalciuria- therefore leading to nephrocalcinosis. You might not be able to explain hypercalciuria but just remember that. Therefore, patients with Bartter's syndrome get hypokalemic metabolic alkalosis. ( as compared to hypokalemic metabolic acidosis in Renal tubular acidosis)

If you are interested to read more about ROMK ( renal outer medullary potassium channel), try to search the net! ( not important in your MRCP!)

As for Gitelman's syndrome, it is an disorder of distal convulated tubule, it is an variant of Bartter's syndome with similar biochemical abnormalities except Gitelman's syndrome has hypocalciuria as compared to hypercalciuria in Bartter's syndrome and hypomagnesimia in Gitelman's syndrome. ( Bartter's syndrome has normal Magnesium Level)

MRCP Past Year Question

A 15-year-old girl is referred to clinic complaining of generalised muscle weakness, fatigue and polyuria. Her blood pressure in clinic is measured at 90/74 mmHg. Investigations:

Serum sodium 127 mmol/l
Serum potassium 3.0 mmol/l
Serum urea 7.2 mmol/l
Serum creatinine 110 umol/l
Serum chloride 92 mmol/l (NR 97-108 mmol/l)
Serum bicarbonate 34 mmol/l (NR 22-28 mmol/l)
82 mmol/l (NR 0.8-1.1 mmol/l)
Urine sodium 160 mmol/l (NR 40-130 mmol/l)
Urine calcium 8.0 mmol/24hr (NR 2.5-8.0 mmol/24hr)
Which of the following is the most likely diagnosis?
Available marks are shown in brackets

1 ) Addison's disease
2 ) Bartter's syndrome
3 ) Laxative abuse
4 ) Liddle's syndrome
5 ) Thiazide diuretic abuse

What is the answer??

Hyperkalemia in MRCP (2)

Hyperkalemia in MRCP (2)

OK, if you are currently working in any hospital around the world, you certainly agree with me that hyperkalemia always disturbs you a lot. I remember that when I was a house officer many years ago, I was once called by staff nurse because she was worried that patient may collapse simply because his Potassium level was 5.4!


I think the general principles of treating hyperkalemia are simple,

First,

You have to act fast to avoid cardiac arrhythmia.

Second,

To shift the Potassium back to the cell ( intracellular) from extracellular ( plasma) if possible.

Third,

To reduce total body Potassium

Fourth,

AND of course, find out the underlying cause of hyperkalemia.


I will not discuss how aggressive you want to treat hyperkalemia and I think it is a judgment call. Anyway, I would be certainly very worried if the Potassium level is more than 6.5 and there is ECG changes. ( Learn about hyperkalemia associated ECG changes, it is a popular question in MRCP).

So, treatment of hyperkalemia can be outlined as below,

I think the very first step to take is to stabilize the heart by giving Calcium gluconate or Calcium chloride. You may want to open your physiology book to learn the mechanism how Calcium acts.

Then ,of course, you want to try to shift back the Potassium back to the cell by giving insulin and glucose. In Malaysia, the combination of insulin, glucose and Calcium therapy in treating hyperkalemia is termed as cocktail regime!

You can also use beta agonist to shift the Potassium back to the cell. Another useful strategy is bicarbonate infusion. Remember, acidosis causes hyperkalemia, therefore alkalosis corrects hyperkaelmia.
Another strategy you may want to try is giving patient cation exchange resin. However, remember that the effect is not immediate, therefore, you have to use previous various strategies to bring down the Potassium level promptly.

Anyway, I must say the most powerful way of treating your hyperkalemia is haemodialysis!!

Hyperkalemia in MRCP (1)

Hyperkalemia in MRCP – Part 1

Electrolyte imbalance is an important topic in MRCP and I think Potassium is the single most important electrolyte in our bodies.

If you are a house officer, I think the commonest electrolyte abnormality you will see in medical ward is hypo/hyperkalemia.

Today, we will discuss about hypokalemia. Before we talk further about causes of hyperkalemia and how do we manage this, we have to learn about basic physiology.



First fact to remember, potassium is mainly intracellular, the concentration of K is about 150mmol/L of H2O inside the cell as compared to about 5 mmol/L outside the cell ( in plasma). Therefore, to maintain this concentration, our body depends greatly on Na-K ATPase channel ( this channel transport 3 Na out of the cell for each 2 K it transports in), however , you must always remember there are H-K ATPASE in specific organs such as kidneys for similar purpose.

Potassium is mainly excreted in kidney although a small proportion is excreted through GIT.

OK, let us talk about causes of hyperkalemia, I can divide them into either increased load, reduced excretion and increased release from cells ( Remember? Potassium is mainly intracellular!)

1) Reduced excretion
Chronic kidney disease ( Potassium is mainly excreted via kidney )
Mineralcorticoid deficiency ( learn the effect of mineralcortiocid on Na-K channel, you will understand)
Some drugs ( especially ACEI/ARB, heparin, potassium sparing drug)

2) Increased load
Overzealous Potassium supplement
Transfusion of blood

3) Increased release from cell
Any causes leading to major cell breakdown such as tumour lysis sundrome, tissue necrosis, rhabdomyolysis
Acidosis ( Remember I told you about H-K pump!!)
Beta blocker

OK, I will talk about management of hyperkalemia in my next post.