Search PubMed⌕ Search

Biomedical subjects

J Henschkowski

Publications and source records attributed to J Henschkowski.

3 recordsLinked to original sources

[Crystalluria].

Crystalluria is often present in routine urinalysis. The precipitation of crystals occurs in supersaturated urine. "Non-specific crystalluria" may be caused by food intake, pH and/or temperature changes of the urine, specially when urine is not analysed immediately. This randomly observed "non-specific crystalluria" is of no clinical value. In contrast, "specific" crystalluria can be associated with diseases such as nephrolithiasis, primary hyperoxaluria or ethylene glycol poisoning. Some drugs are excreted as crystals and may cause heavy crystalluria leading to kidney injury; this is the case of retroviral drugs and some antibiotics used in clinical practice. In these situations the diagnosis can be made by urinalysis and therapy be adapted accordingly. Important for the analysis of crystalluria is the correct handling of the fresh urine, knowledge of urinary pH and, of course, training in microscopic techniques.

Crystallization↗

[Edema and the nephrotic syndrome].

If proteinuria is of sufficient amount, and persists for long enough, then a series of consequences arises which is called the nephrotic syndrome. The most notable consequence of massive proteinuria is salt and water retention leading to edema formation. This edema is found in association with proteinuria usually greater than 3.5 g/day, accompanied by hypoalbuminemia, usually less than 25 g/l. The underlying disease is usually a glomerulonephritis, albeit in rare situations severe renal artery stenosis can lead to proteinuria by hyperfiltration. Two theories have been proposed. In the classical "underfill" theory edema is considered to be secondary to salt retention resulting from renal hypoperfusion. According to this theory the primary event is the decrease in plasma volume due to the diminution of plasma oncotic pressure resulting from hypoalbuminemia, causing transfer of fluid from the plasma to the interstitial space "underfilling" the blood compartment and resulting to secondary renal sodium retention. This mechanism applies mainly to the nephrotic syndrome associated with minimal change disease observed in children. By contrast, in most adults with the nephrotic syndrome due to minimal change disease or other glomerular lesions such as membranous or proliferative glomerulonephritis, an initial plasma volume expansion is observed. Therefore, the primary event responsible for the sodium retention is a renal intrinsic excretory defect, which leads to extracellular fluid expansion and edema formation. Therapy is specific for the specific glomerular disease and symptomatic for the edema (diuretics), anticoagulation therapy for prevention of venous thrombosis and embolism, antibiotics for infections, and most of all, omission of triggering factors such as specific xenobiotics.

Adult↗

Treatment of severe hyponatremia: conventional and novel aspects.

Hyponatremia is a frequent electrolyte disorder. A hyponatremia is called acute severe (<115 mM) when the duration has been <36 to 48 h. Such patients often have advanced symptoms as a result of brain edema. Acute severe hyponatremia is a medical emergency. It should be corrected rapidly to approximately 130 mM to prevent permanent brain damage. In contrast, in chronic severe hyponatremia (>4 to 6 d), there is no brain edema and symptoms are usually mild. In such patients, a number of authors have recommended a correction rate <0.5 mM/h to approximately 130 mM to minimize the risk of cerebral myelinolysis. Sometimes it is not possible to diagnose whether a severe hyponatremia is acute or chronic. In such cases, an initial imaging procedure is helpful in deciding whether rapid or slow correction should be prescribed. The modalities of treatment of severe hyponatremia have so far consisted of infusions of hypertonic saline plus fluid restriction. In the near future, vasopressin antagonists will become available. Preliminary experience has already demonstrated their efficiency of inducing a sustained water diuresis and a correction of hyponatremia.

Acute Disease↗