Podocytes structure and function in Kidney

The podocyte is the largest cell in the glomeruli. It has a highly specialized three dimensional structure and a unique molecular profile closely related to the basic functions it performs. Podocytes are large octopus shaped cells similar to GBM.

Transmission of Electronic Microscopy and Scanning Electron Microscope (SEM) presented its unique and complex structure. Three main structural domains have been identified: cell body, cellular processes and foot processes. The body of a cell is usually located in a valley created by the reflection.of adjacent capillary loops.

The body of the cell contains the nucleus and other organelles as abundance of the endoplasmic reticulum, the large Golgi apparatus, mitochondria and excessive amount of lysosomes . Sometimes the rudimentary cilia are also present protruding from the surface. The body of the cell is not based directly on GIN. It is separated from the CBM by the subpodocyte space and layer on foot processes.

Subpodocyte space can be a dynamic compartment that can vary in volume, limit the movement of the ultrafiltrate in the urinary space, and provide a mechanism for the involvement of podocytes in the modulation of Capillary permeability and podocyte response to injury. Long, thin, arborizing cellular processes projecting from the cellular bodies.


 Podocytes structure and function in Kidney



These processes contain several organelles but are rich in microtubules and intermediate filaments that are parallel to the longitudinal axis. They can branch into secondary or tertiary cellular processes before investing several capillary loops. Cellular processes ultimately lead to finite structures called foot processes or pedicels.

It is difficult to differentiate the function of podocytes as they are still mysterious type of cells. Normally, they are categorized as modified form of pericytes having specialized intracellular junctions e.g slit diaphragm. As a supportive cell it also contributes in para-cellular permeability control. The most import function  is acting as barrier of glomerular filter.


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Hyperpyrexia Symptoms, Causes, Treatment, Management and Guidelines

Hyperpyrexia is an emergency condition where the body temperature rise above normal. Another name fore hyperpyrexia is hyperthermia. This happens when the body temperature of an infected person rise abnormally to a temperature range of about 106.7℉ and which is not due to any physical or mechanical activities. At most time, the increase in temperature happens when the part of the brain that controls the body temperature is unable to function to it best, as a result of infection, cerebral injury, trauma or due to side effect of some drugs. This increase in temperature triggers raise in muscle tightening, and therefore causes a feeling of cold in such a person experiencing hyperpyrexia.

Typically, body temperature is being regulated within a narrow range, which fluctuates predictably continusoly to adjust accordin to ambient temperature. Compensatory mechanisms for temperature regulation provide a thermal homeostasis via autonomic nervous control e.g altered muscle tone, shunt blood flow to and from peripheral vascular beds, and causing heat or heat seeking behavior.

Exogenous substances as components of the bacterial cell wall (lipopolysaccharides ), degradation products, bacterial endotoxins, drugs, immune complexes and complement factors induce activated polymorphonuclear cells to release a group of endogenous pyrogens cytokines . These cellular mediators, known as interleukins (IL) -1 and IL-6, tumor necrosis factor (TNF), and interferon G induce the production of prostaglandin E2 (PGE2) by endothelial cells. In the vascular region of the prepoptic nucleus of the anterior hypothalamus, PGE2 diffuses the short distance between the neurons of the temperature control center.


Hyperpyrexia Symptoms, Causes, Treatment, Management and Guidelines

Hyperpyrexia Symptoms


Symptoms of Hyperpyrexia include an uncontrollable increase in the body’s temperature due to inability of the body to regulate the body temperature to its normal state. Other symptoms include cold, loss of appetite, pains in the whole body or some body joints, headache and some unusual circumstances like vomiting (this usually happens in children of tender age.

Hyperpyrexia Causes


Hyperpyrexia is mainly caused by the inflammation in part of the brain called hypothalamus, which is responsible for the regulation of the body temperature. This inflammation may be associated with infection, cerebral injury, mechanical injury, trauma or accidental damage. Hyperpyrexia may also be idiopathic in nature mean it belong to unknown origin. However, it is commonly observed that some drugs like anesthetics, deploarizing agents and

Hyperpyrexia Treatments


Hyperpyrexia is an emergency medical condition. Treatment goes for the lessening of the body temperature to 39℃. Patient should be covered with wet sheets or towels and splashed with icy water while air is blown or fanned over him to advance evaporative cooling. As an option, the patient might be drenched in chilly water. The appendages are delicately kneaded to advance dissemination. At the point when the body temperature fall to 38 degrees, the patient should be shifted to a cool room and looked for further ascent of temperature.

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Xanthochromia csf Definition, Test, Timing, Guidelines, Interpretation

The presence of red blood cells in cerebrospinal fluid (CSF), WBC's, increased protein concentration in CSF and xanthochromia are important findings for the detection of vascular neurological disorders. However, diagnostic information from these results is often insufficiently matched despite the addition of other clinical data. The introduction of cranial CT-Scan is an extremely useful for the detection of vascular lesions, including intracranial hemorrhage and stroke.

Unfortunately, the necessary equipment is quite complicated and expensive and for now it is only available in larger medical centers. Moreover, bleeding near bone structures such as subarachnoid hemorrhage (SAH) may escape diagnosis and hemorrhagic component in cerebral infarctions may be difficult to detect by CT-Scan. Xanthochromia of CSF microscopically observed as discoloration of the Yellowish supernatant with variations to a reddish or brownish color and is generally accepted as a sign of lesion bleeding.

Xanthochromia  of cerebrosponal fluid develops for several hours after bleeding in older children and adults.It is commonly observed that adults with sub-arachnoid hemorrhage develops xanthochromia within 12 hours of ictus or stroke. The identification of xanthochromia in newborns has not been systematically studied well but it happened Slower than older patients.



This slow change may refer to a delay in the induction of the oxyanganase enzyme, which is present in the subarachnoid membrane and is responsible for the conversion of hem to bilirubin, the major pigment of xanthochromia in CSF. In a recent study it has been observed that activity of hem oxygenase reached peak Values ​​at 6 to 12 hours after injection of hem in the subarachnoidial space . Determining the presence of xanthochromia in newborn is sometimes difficult in the presence of elevated serum bilirubin.

Xanthochromia  Test, Timing, Guidelines, Interpretation


Xanthochromia as pink or yellow tint in the cerebrospinal fluid does not rule out the possibility of subarachnoid hemorrhage (SAH). Xanthochromia may reflects hemoglobin degradation and is present anywhere from 6 to 12 hrs after sub-arachnoid hemorrhage. The absence of xanthochromia does not rule out the possibility of sub-arachnoid hemorrhage if the patient presents more than 2 weeks after the onset of headache.

Xanthochromia is measured by visual inspection or by spectrophotometry. Most hospitals measure by visual inspection, which is obviously a much less sensitive test. Xanthochromia happened due to hyperbilirubinemia, accidental hemorrhage or encephalitis might require further unnecessary diagnostic studies. Additional cerebrospinal  studies should be kept in considered in case of ambiguous findings, especially if the patient has been in an endemic area or has compromised immune system.

Xanthochromia visibility in CSF might be due to the following:
  1. Oxyhemoglobin as a result of lysis of red blood cells 
  2. Bilirubin (bilirhachia) in patients with jaundice.
  3. CSF protein levels above 150 mg / dL, which are also present in bloody traumatic taps or pathological conditions such as complete spinal blockade or spinal stenosis, poly-neuritis, and meningitis.
  4. Merthiolate disinfectant contamination 
  5. Carotenoids in people with hypercarotenemia (i.e., hypervitaminosis A).
  6. Melanin (brown) of meningial metastatic melanoma.
  7. Rifampin therapy (red-orange).
Spectrophotometry can also help to distinguish hemoglobin from other xanthochromic pigments with maximum absorption peaks.
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