Interstitial cells of the renal medulla

doi:10.1016/S0022-5320(66)80129-6

Journal of Ultrastructure Research

Volume 15, Issues 5–6, August 1966, Pages 589-613

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Interstitial cells in the medulla of the rat kidney have been studied by electron microscopy after fixation by perfusion with glutaraldehyde. In the outer zone of the medulla the interstitial cells resemble fibroblasts and are associated with collagen and a small amount of ground substance.

In the inner zone of the medulla the interstitial cells have some characteristics of fibroblasts, but also show several unusual features. They have remarkably enlarged perinuclear cisternae. Groups of vesicles are found outside cells, and may be associated with apparent gaps in the plasma membrane. The cells and their processes are more closely related to capillaries and thin limbs of the loop of Henle than to collecting tubule cells. The most prominent feature of the interstitial cells of the inner medulla is their content of numerous osmiophilic droplets of unknown function.

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Cited by (56)

A Cumulative Shear Mechanism for Tissue Damage Initiation in Shock-Wave Lithotripsy
2007, Ultrasound in Medicine and Biology
Citation Excerpt :
However, data indicate that it too has a long relaxation time. The notable lack of collagen fibers (Osvaldo and Latta 1966) in kidney interstitial gel would suggest that its elasticity would be particularly small, even for interstitial gels. Zeng et al. (2006) studied a collagen gel in a rheometer and fit results with a generalized Maxwell viscoelastic model with two relaxation times: λ1 ∼ 0.6 s and λ2 ∼ 5 s.
Evidence suggests that inertial cavitation plays an important role in the renal injury incurred during shock-wave lithotripsy. However, it is unclear how tissue damage is initiated, and significant injury typically occurs only after a sufficient dose of shock waves. Although it has been suggested that shock-induced shearing might initiate injury, estimates indicate that individual shocks do not produce sufficient shear to do so. In this paper, we hypothesize that the cumulative shear of the many shocks is damaging. This mechanism depends on whether there is sufficient time between shocks for tissue to relax to its unstrained state. We investigate the mechanism with a physics-based simulation model, wherein the basement membranes that define the tubules and vessels in the inner medulla are represented as elastic shells surrounded by viscous fluid. Material properties are estimated from in-vitro tests of renal basement membranes and documented mechanical properties of cells and extracellular gels. Estimates for the net shear deformation from a typical lithotripter shock (∼0.1%) are found from a separate dynamic shock simulation. The results suggest that the larger interstitial volume (∼40%) near the papilla tip gives the tissue there a relaxation time comparable to clinical shock delivery rates (∼1 Hz), thus allowing shear to accumulate. Away from the papilla tip, where the interstitial volume is smaller (∼20%), the model tissue relaxes completely before the next shock would be delivered. Implications of the model are that slower delivery rates and broader focal zones should both decrease injury, consistent with some recent observations. (E-mail: [email protected])
Anatomy of the renal interstitium
1991, Kidney International
The interstitium of the kidney comprises the extravascular intertubular spaces of the renal parenchyma, with their attendant cellular elements and extracellular substances. As we define it here, the interstitium is bounded on all sides by tubular and vascular basement membranes. This suggests including the lymphatics within the interstitium. That the vascular compartment on the other hand should be distinguished from the interstitium—in contrast to what is often assumed—is suggested by evidence of significant solute polarization between capillary plasma and the interstitium [1].
The interstitium of the kidney is not a simple passive space in which the “true” functional units—nephrons and vessels—are embedded. Rather, it mediates and in fact modulates almost all exchange among the tubular and vascular elements of the renal parenchyma; along with segmental specialization of the nephron, it underlies the functional zonation of the kidney; it probably influences glomerular filtration through its effects on tubuloglomerular feedback; it decisively affects growth and differentiation of parenchymal cells; it determines the compliance of the peritubular micro vasculature; the cells of the interstitium produce a variety of local (autocoid) and systemic hormones; and alterations in the interstitium contribute to the clinical manifestations of renal disease.
This review will deal with the various cellular and extracellular elements of the renal interstitium under normal conditions. The studies on which our conclusions are based were conducted principally in experimental animals, in particular the rat.
Development of the human renal inner medullary interstitial cells
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Two cell types were identified in the inner medulla and papilla of four fetal kidneys of 16 1/7-, 17 3/7-, 21 1/7-and 25 5/7-week-old (menstrual): undifferentiated mesenchymal cells and some highly differentiated cells which contained some lipid granules, lysosomes, smooth and rough endoplasmic reticulum. The structure of these cells resembled the two cell types which were observed in the adult tissue.
Experimental analgesic nephropathy: Changes in renal structure and urinary concentrating ability in fischer 344 rats given continuous low doses of aspirin and paracetamol
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Long-term treatment with aspirin and paracetamol produced renal papillary necrosis in female Fischer 344 rats. Aspirin (230 mg/kg body weight/day) and paracetamol (380 mg/kg body weight/day) were dissolved in drinking water and given continuously for up to 65 weeks.
Renal morphological changes were examined between 21 weeks and 65 weeks of commencement of analgesic treatment using light and electron microscopy, and were compared with age-matched controls. Structural damage initially occurred in the mid-papillary region, and specifically involved the interstitial cells and interstitial matrix. Necrosis of the epithelium of the thin limbs of the loop of Henle was present only after interstitial changes were well established. Cortical interstitial fibrosis and tubular atrophy occurred after renal papillary changes were observed. There was no evidence of significant vascular damage.
Urinary concentrating ability was measured sequentially during the period of analgesic treatment. A decrease in urine concentrating ability was present when early changes to the interstitial cells and matrix were observed, and concentrating ability continued to decrease in parallel with increasing morphological damage.
This study describes an animal model of analgesic-induced nephropathy, enabling early morphological changes to be studied and correlated with renal functional changes.
Fluorescent probes for understanding the mechanisms of chemically induced cellular injuries
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Ultrastructural study of ochratoxicosis in quail (Coturnix coturnix japonica)
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Ultrathin sections of liver and kidney from 11-week-old quail fed, from day-old, ochratoxin A (oa) (mixed in the diet at levels of 4 and 8 ppm) were examined in the electron microscope. Pathological changes in the kidneys were limited to the proximal convoluted tubules (pct) and glomeruli. In the pcts, abnormal mitochondria and excessive numbers of lipid droplets were the principal findings with glomeruli showing thickened basement membranes. Swollen mitochondria and variable glycogen deposition were the chief features present in the livers. It is suggested that oa is more hepatotoxic in quail than in broilers, as well as being nephrotoxic.

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¹: This investigation was supported by Research Grant No. AM-06074 from the National Institute of Arthritis and Metabolic Diseases, U.S. Public Health Service.

²: Present address: Department of Pathology, Karolinska Sjukhuset, Stockholm, Sweden.

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Interstitial cells of the renal medulla1

J. Ultrastruct. Res.

J. Ultrastruct. Res.

Exptl. Neurol.

Exptl. Cell Res.

Exptl. Mol. Pathol.

Am. J. Med.

J. Ultrastruct. Res.

J. Ultrastruct. Res.

Am. J. Med.

S. Afr. J. Med. Sci.

Anat. Record

J. Anat.

J. Cell Biol.

J. Biophys. Biochem. Cytol.

Physiol. Bohemoslov.

J. Biophys. Biochem. Cytol.

J. Cell Biol.

Am. J. Med.

J. Cell Biol.

Z. Physiol. Chem.

J. Biophys. Biochem. Cytol.

Some Cytologic Effects of Antibodies

Lab. Invest.