Nephrology pearls

Erythropoietin: (EPO) may cause seizures occurs after 90 days from starting the treatment

Erythropoietin (EPO) use may cause secondary iron deficiency

If anemic patient with renal failure failed to response to erythropoietin treatment then think of:

1-      Iron deficiency

2-      Inadequate dose

3-      Concurrent infection or inflammation

4-      Hyperparathyroid bone disease

5-      Aluminum toxicity

Indication for Urgent Dialysis:

•Severe acidosis

•Pulmonary edema due to volume overload

•Hyperkalemia

•Uremic pericarditis

•Severe uremic symptoms (encephalopathy, vomiting, .. )

Risk factors for renal Stones:

•Dehydration

•Hypercalciuria, hyperparathyroidism, hypercalcemia

•Cystinuria (NOT CYSTINOSIS)

•High dietary oxalate

•Renal tubular acidosis

•Medullary sponge kidney, polycystic kidney disease

•Beryllium or cadmium exposure

•Gout (urate stones)

• Ileostomy: Ileostomy can cause loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid and that can cause urate renal stones

Loop diuretics, steroids, acetazolamide and theophylline all promote calcium renal stones

Thiazides diuretics can prevent calcium stones by increasing distal tubular calcium resorption

Causes of sterile pyuria:

-Partially treated urinary tract infection (UTI)

-Urethritis e.g. Chlamydia, TB and ureaplasma urealyticum

-Renal tuberculosis

-Renal stones

-Appendicitis

-Bladder or renal cell cancer

-Adult polycystic kidney disease

-Analgesic nephropathy

In patient with 'Musty' odor to urine and sweat think of Phenylketonuria

In Homocystinuria there is downwards dislocation of lens

In Marfan syndrome there is upward dislocation of lens

Benign prostatic hyperplasia (BPH) is not risk factor for prostate cancer

Nephrotic syndrome causes marked proteinuria and loss of antithrombin III and plasminogen in the urine thus leading to increased risk of arterial and venous thrombosis.

Nephrotic Syndrome:

Triad of

1. Proteinuria (> 3g/24hr) causing

2. Hypoalbuminemia (< 30g/L) and

3. Edema

Membranous glomerulonephritis

Cause: infections, rheumatoid drugs, malignancy

1/3 resolve, 1/3 respond to cytotoxins, 1/3 develop chronic renal failure

Causes of membranous nephropathy:

- Autoimmune disease, such as lupus erythematosus

- Infection: hepatitis B, hepatitis C or syphilis

- Certain medications, such as gold salts and nonsteroidal anti-inflammatory drugs

- Solid cancerous tumors or blood cancers (Lymphoma)

- Diabetes

Mesangioproliferative glomerulonephritis

IgA nephropathy

Usually young adult with painless hematuria following an upper respiratory tract infection (URTI)

Fibrillary glomerulonephritis (FGN)

associated with hepatitis C virus infection and with malignancy and autoimmune disease.

Deposition of IgG and infiltrative fibrils

The signs and symptoms include

Hematuria

Proteinuria

Treatment is generally determined by the severity of the kidney problem

Diffuse proliferative glomerulonephritis

Classically:  comes in child, post streptococcal infection

Most common form of renal disease in Systemic lupus erythematosus (SLE)

Glomerulonephritis and low serum C3 levels can be seen in:

Post streptococcal glomerulonephritis

Subacute bacterial endocarditis

Systemic lupus erythematosus

Mesangiocapillary glomerulonephritis

Causes of blue greenish urine:

-Pseudomonas infection

-Blue diaper syndrome and Hartnup disease are autosomal recessive disorders in which tryptophan builds up in the GI tract, causing bacteria to metabolize it to indole, leading to a buildup of indican in the urine.

-Familial benign hypercalcemia, a rare inherited disorder, is sometimes called blue diaper syndrome because children with the disorder have blue urine.

-And some drugs

Drugs that may cause green urine are:
Cimetidine
Promethazine
Amitriptyline
Flutamide
Indomethacin
Methocarbamol
Methylene blue
Mitoxantrone
Propofol
Phenylbutazone
Triamterene

Drugs that may cause orang color urine:

Idarubicin

Ferrioxamine

Oxamniquine

Phenazopyridine

Rifampicin

Warfarin

The causes of reduced urea to creatinine ratio include:

Low protein diet

Malnutrition

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Pregnancy

Severe Liver Dysfunction

Rhabdomyolysis

Rheumatoid arthritis can lead to secondary amyloidosis, it may complicated with nephrotic syndrome

In nephrotic syndrome due to amyloidosis, renal biopsy will show deposits in the mesangium and capillaries which stain pink with congo red and appear as green birefringence when under polarised light.

Bartters syndrome is a combination of juxtaglomerular hyperplasia, hyperaldosteronism, hypokalemic, and hypochloremic alkalosis often with hypercalciuria.

It can lead to renal stones due to the hypercalciuria.

  

Polycystic kidney disease

Can be ether:

Autosomal dominant polycystic kidney disease (ADPKD) 

Or 

Autosomal recessive polycystic kidney disease (ARPKD)

And in rare cases can be due to genetic mutation occurs on its own (spontaneous)

Complications associated with polycystic kidney disease include:

-Renal failure

-High blood pressure

-preeclampsia in pregnant women

-Liver cyst

-Brain aneurysm

-Heart valve abnormalities (MVP)

-Colon problems (diverticulosis)

-Chronic pain

Alport syndrome:

Hematuria and proteinuria

Sensorineural hearing loss

Leiomyomatosis

Eye abnormalities: because Alport syndrome is caused by a collagen defect in the basement membrane of the kidneys which can also be found in the ear, cornea, lens capsule and retina

Fanconi syndrome is a disorder of the kidney tubes in which certain substances normally absorbed into the bloodstream by the kidneys are released into the urine instead that results in excess amounts of glucose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, and certain amino acids being excreted in the urine

Osteomalacia is a common presenting feature in adults with Fanconi syndrome due to the loss of excessive calcium and phosphate and a defect in the hydroxylation of 25 hydroxyvitamin D

Glucose freely filtered at glomerulus and reabsorbed in proximal tubule

Causes of renal glycosuria:

Pregnancy      

Fanconi syndrome      

Wilson’s disease         

Cystinosis       

Lead poisoning

Hereditary tyrosinemia

oculocerebrorenal syndrome (Lowe syndrome).

GFR decreases with age but would not be reflected as a rise in serum creatinine due to the age associated decline in muscle mass

False results in creatinine measurement:

Very high bilirubin level causes creatinine to be falsely low

Ketone body (acetoacetate) and certain drugs (cefoxitin) create falsely high creatinine levels

Urea is the major end product of protein metabolism

Urea production reflects dietary intake of protein and catabolic rate.

Increased protein intake or catabolism (sepsis, trauma, GI bleed) causes urea level to rise

Ketones can be found in urine in case of alcoholic or diabetic ketoacidosis, prolonged starvation, fasting, pregnancy, dehydration and with some medications, such as corticosteroids and diuretics

Antidiuretic hormone ADH, also called vasopressin, arginine vasopressin or argipressin, is stimulated by hypovolemia; when hypovolemia is rapidly corrected, the ADH level may falls suddenly causing sudden brisk water diuresis, and therefore rapid rise in serum Na+ level

Nephrogenic diabetes insipidus (DI):

Lithium is the most common cause, other causes include hypokalemia, hypercalcemia, and congenital

Diabetes insipidus (DI):

Serum vasopressin concentration may be absent or low (in central DI), or elevated (in nephrogenic DI)

Renal artery stenosis causes:

Atherosclerotic plaques, about 90%, proximal 1/3 renal artery, usually males >55 years, smokers

Fibromuscular dysplasia: about 10%, distal 2/3 renal artery, may be segmental branches, usually young females, onset <30 years

Decreased renal perfusion of one or both kidneys leads to increased renin release and that cause increased angiotensin production which raises blood pressure in two ways

1. Causes generalized arteriolar constriction

2. Increase Na+ and water retention via release of aldosterone

Nonsteroidal anti-inflammatory drugs (NSAIDs) induced acute kidney injury (AKI)

Prostaglandins vasodilate afferent renal arteriole to maintain blood flow

NSAIDs preventing prostaglandin synthesis by blocking cyclooxygenase enzyme, thereby causing renal ischemia and pre renal azotemia

Acetaminophen induced nephropathies

Acetaminophen can cause Acute Tubular Necrosis due to both direct toxicity and ischemia

Renal function spontaneously returns to baseline within 1-4 weeks

Dialysis may be required during the acute episode of ingestion

Papillary Necrosis

Type 1 DM susceptible to ischemic necrosis of medullary papillae causing papillary necrosis DM induced nephropathies

It can present as renal colic with or without hydronephrosis

Polycystic kidney disease

Extra renal manifestations of polycystic kidney disease include multiple asymptomatic hepatic cysts, mitral valve prolapse, cerebral aneurysm, diverticulosis, and less common cysts in pancreas, spleen, thyroid, ovary, aorta and seminal vesicles

Medullary sponge kidney

About 10% of patients who present with renal stones have medullary sponge kidney

The serum creatinine may not change much during acute renal failure in patients with decreased

muscle mass. Urinalysis, a simple and easy test, often provides the specific diagnosis.